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Sara Dorri , Alireza Atashi , Safoura Dorri , Ebrahim Abbasi , Mohsen Alijani-Zamani , Najme Nazeri ,
Volume 74, Issue 10 (1-2017)
Volume 74, Issue 10 (1-2017)
Abstract
Background: There is no need to explain the importance of collection, recording and analyzing the information of disease in any health organization. In this regard, systematic design of standard data sets can be helpful to record uniform and consistent information. It can create interoperability between health care systems. The main purpose of this study was design the core dataset to record colorectal cancer information in Iran.
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Methods: For the design of the colorectal cancer core data set, a combination of literature review and expert consensus were used. In the first phase, the draft of the data set was designed based on colorectal cancer literature review and comparative studies. Then, in the second phase, this data set was evaluated by experts from different discipline such as medical informatics, oncology and surgery. Their comments and opinion were taken. In the third phase refined data set, was evaluated again by experts and eventually data set was proposed. Results: In first phase, based on the literature review, a draft set of 85 data elements was designed. In the second phase this data set was evaluated by experts and supplementary information was offered by professionals in subgroups especially in treatment part. In this phase the number of elements totally were arrived to 93 numbers. In the third phase, evaluation was conducted by experts and finally this dataset was designed in five main parts including: demographic information, diagnostic information, treatment information, clinical status assessment information, and clinical trial information. Conclusion: In this study the comprehensive core data set of colorectal cancer was designed. This dataset in the field of collecting colorectal cancer information can be useful through facilitating exchange of health information. Designing such data set for similar disease can help providers to collect standard data from patients and can accelerate retrieval from storage systems. |
Elham Hoveizi , Tayebeh Mohammadi ,
Volume 74, Issue 11 (2-2017)
Volume 74, Issue 11 (2-2017)
Abstract
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Background: One of the major causes of death in the world is cancer and therefore any study in the field of cancer biology is of great importance. Head and neck cancers represent approximately 2-5% of neoplasms which is higher in some countries. The most appropriate therapy for various cancers is identifying effective and efficient ways that contribute to initiation of apoptosis. Cyclophosphamide is an alkylating agent that stops the replication of DNA and then, it stops the cell proliferation and viability. Therefore, cyclophosphamide is used to treat various types of cancer. In this study we evaluate the cytotoxic effects of cyclophosphamide on viability of (head and neck cancer cells) HN5 cell line and compare it with fibroblast cells as noncancerous cells. Methods: This experimental study was done in cell and developmental laboratory in faculty of science, Shahid Chamran University of Ahvaz in Spring of 2016. HN5 cell line and embryonic fibroblast cells were grown in DMEM supplemented with 10% fetal bovine serum (FBS), penicillin/streptomycin (100 U/ml, 100 µg/ml) at 37 °C, then the effects of different concentrations of cyclophosphamide on cell viability was evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. 4',6-diamidino-2-phenylindole (DAPI) staining was performed to determine the proportion of apoptotic cells by manually counting pyknotic nuclei. According to standard procedures from day 13 embryos of outbred strains naval medical research institute (NMRI), fibroblast cells were isolated. In this study HN5 cell line and fibroblasts were exposed to cytostatics for 72 hours. Results: Various concentrations of cyclophosphamide were effective in cytotoxicity of HN5 cancer and fibroblast cells. A significant cytotoxicity was observed with the examined concentration of 1 µg/ml of cyclophosphamide with 50% in 3th day and P< 0.001. Interestingly, at low concentrations, cyclophosphamide was more toxic than at higher concentrations. Conclusion: Totally cyclophosphamide had low toxicity effects on both of the cell lines but the toxicity effects of cyclophosphamide on HN5 were significantly greater than fibroblast cells. These results indicate that cyclophosphamide can be a potential anticancer agent. |
Arash Salmaninejad , Parisa Kangari , Abbas Shakoori ,
Volume 75, Issue 1 (4-2017)
Volume 75, Issue 1 (4-2017)
Abstract
Breast cancer is the most commonly diagnosed cancer in women worldwide. Enormous advancement has been made over the last decades in understanding the biology of breast cancer. Nevertheless, the molecular mechanisms regulating progression, gaining of invasive and metastatic phenotypes, and therapeutic resistance are still not completely understood. Oxidative stress initiate by disbalance in redox status of body. In this case, increase of free radicals in body cause tissue damage. One of the significant species of free radicals is reactive oxygen species (ROS) that produced by various metabolic pathways, comprising aerobic metabolism in the mitochondrial respiratory chain. They play a serious role in cellular physiology and pathophysiology likewise beginning and evolution of numerous types of cancers. ROS overproduction is deleterious to cells, and considered key-factors for the development of numerous diseases, such as cardiovascular disorders, neurodegenerative diseases, and cancer. Cancer cells are commonly submitted to upper ROS levels that further incite malignant phenotype through motivation to preserved proliferation, angiogenesis, death evasion, invasiveness, and metastasis. ROS impress various signaling pathways, comprising mitogenic pathways and growth factors, and also controls numerous cellular processes, containing cell proliferation, thus stimulates the undisciplined growth of cells which inspires the development of tumors and initiates the progression of carcinogenesis. The importance of ROS on breast cancer development and etiology is being increasingly clarified. Nevertheless, fewer consideration has been given to the progress of redox system-targeted strategies for breast cancer treatment. Augmented oxidative stress caused by reactive species can diminish the body’s antioxidant defense against angiogenesis and metastasis in cancer cells. These processes are core factors in the development of cancer. Bimolecular reactions cause free radicals which create such compounds as malondialdehyde (MDA) and hydroxyguanosine. These substances known as indicators of cancer. In this review, free radicals as oxidizing agents, antioxidants as the immune system, and the role of oxidative stress in cancer, particularly breast cancer, have been investigated by hope that better exploration of the factors involved in the occurrence and spread of cancer will improve the identification of treatment aims.
Mahshid Hatami , Mohammad Esmaeil Akbari , Morteza Abdollahi , Marjan Ajami , Yasaman Jamshidinaeini , Sayed Hossein Davoodi ,
Volume 75, Issue 1 (4-2017)
Volume 75, Issue 1 (4-2017)
Abstract
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Background: Breast cancer is the most common cancer among females in the world. Identifying the nutrients that modify the risk of the disease is one of the key strategies for improving the quality of life and reducing treatment costs. Epidemiological studies support the role of macronutrients and vitamins involved in one carbon metabolism in the etiology of the disease. This study aimed in investigation of the relationship between the intake of macronutrients and vitamins involved in one carbon metabolism with breast cancer risk. Methods: This case-control hospital base study was conducted at Shohada Hospital, Tehran from April to February 2015. Demographic data, physical activity level and nutrients’ intake from diet and supplements were collected through interview from 151 cases and 154 controls. Dietary intake was assessed by a valid and reliable 168-item semi-quantitative food frequency questionnaire. Then intake of macronutrients and B vitamins was assessed by Nutritionist 4 software (First Databank Inc., CA, USA). Comparing categorical variables between the two groups was done by Chi-squared test and the relationship between intake of studied nutrients and risk of breast cancer was determined using logistic regression test. Results: There were no difference in age, menarche age, menopause age, body mass index (BMI), number of live births between two groups. But the difference in physical activity, energy intake, marital status, educational level, occupation, oral contraceptives use was significant (P< 0.001). After modifying the effects of confounding variables, the risk of breast cancer was significantly lower in the highest intake quartile category relative to the lowest quartile category for total protein, total fiber, intake of vitamins B2, B6, B12 and folate (Ptrend< 0.001). Before modifying the effects of confounding variables, the risk of breast cancer was significantly higher in the highest intake quartile category relative to the lowest quartile category for carbohydrate and fat; but after modifying the effects of confounding variables, results were not significant. |
Conclusion: The results showed that high intake of protein, fiber, vitamins B2, B6, B12 and folate are associated with lower risk of breast cancer.
Mehrdad Khatami, Sam Kharazi , Zeinab Kishani Farahani , Hakim Azizi , Marcos Augusto Lima Nobre,
Volume 75, Issue 1 (4-2017)
Volume 75, Issue 1 (4-2017)
Abstract
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Background: The modern science of nanotechnology is an interdisciplinary science that has contributed to advances in cancer treatment. This study was performed to evaluate the therapeutic effects of biosynthesized silver nanoparticles on breast cancer cell of line MCF-7 in vitro. Methods: This analytical study was performed in Kerman and Bam University of Medical Sciences, Bam City, Kerman Province, Iran from March 2015 to March 2016. Silver nanoparticles suspension was synthesized using palm kernel extract. The resulting silver nanoparticles were studied and characterized. The ultraviolet-visible spectroscopy and transmission electron microscopy used for screening of physicochemical properties. The average particle size of the biosynthesized silver nanoparticles was determined by transmission electron microscopy. The properties of different concentrations of synthesized silver nanoparticles (1 to 3 μg/ml) and palm kernel extract (containing the same concentration of the extract was used for the synthesis of silver nanoparticles) against MCF-7 human breast cancer cells were determined by MTT assay. MTT is used to assess cell viability as a function of redox potential. Actively respiring cells convert the water-soluble MTT to an insoluble purple formazan. Results: The ultraviolet-visible spectroscopy showed strong absorption peak at 429 nm. The X-ray diffraction (XRD) and transmission electron microscopy (TEM) images revealed the formation of silver nanoparticles with spherical and octagon shape and sizes in the range between 1-40 nm, with an average size approximately 17 nm. The anti-cancer effect of silver nanoparticles on cell viability was strongly depends on the concentration of silver nanoparticles and greatly decrease with increasing the concentration of silver nanoparticles. The IC50 amount of silver nanoparticle was 2 μg/ml. Conclusion: The biosynthesized silver nanoparticles showed a dose-dependent toxicity against MCF-7 human breast cancer cells. |
Mina Golmohammadi , Hamid Asadzadeh Aghdaei , Hossein Maghsoudi , Ehsan Nazemalhosseini Mojarad,
Volume 75, Issue 5 (8-2017)
Volume 75, Issue 5 (8-2017)
Abstract
Background: Most of colorectal cancers (CRC) have originated from intestinal polyps. Evaluating of the expression level of genes that are involved in tumors growth and development, may consider as diagnostic factor of malignancy in the polyps. AXIN2 regulates the level of nuclear β-catenin in a negative-feedback loop there by being a negative regulator and target gene at the same time. The aims of current study were to examine the expression level of the AXIN2 in the colonic polyps and its linkage with the pathological features of the polyps.
Methods: In the present analytical-descriptive study, the investigated population was chosen from the cases with colonic polyps that referred to the Gastroenterology and Liver Diseases Research Center, Taleghani Hospital, Tehran, Iran, from October 2014 to April 2015. Forty four biopsy polyp samples and 10 normal tissue samples were collected, as well as the demographic and clinical properties of the patients and the expression level of AXIN2 gene was quantified by Real-time PCR. The outcomes were analyzed by the ABI Prism 7500 Sequence Detection System (SDS) software, version 2.1.0 (Applied Biosystems Inc., Foster City, CA, USA) and GraphPad Prism, version 3 (GraphPad Software Inc., La Jolla, CA, USA) Also, the expression changes of the intended gene in target groups were compared with the normal tissues using the 2-ΔΔCt equation.
Methods: In the present analytical-descriptive study, the investigated population was chosen from the cases with colonic polyps that referred to the Gastroenterology and Liver Diseases Research Center, Taleghani Hospital, Tehran, Iran, from October 2014 to April 2015. Forty four biopsy polyp samples and 10 normal tissue samples were collected, as well as the demographic and clinical properties of the patients and the expression level of AXIN2 gene was quantified by Real-time PCR. The outcomes were analyzed by the ABI Prism 7500 Sequence Detection System (SDS) software, version 2.1.0 (Applied Biosystems Inc., Foster City, CA, USA) and GraphPad Prism, version 3 (GraphPad Software Inc., La Jolla, CA, USA) Also, the expression changes of the intended gene in target groups were compared with the normal tissues using the 2-ΔΔCt equation.
| Results: The data showed enhanced level of the expression of AXIN2 gene in the colonic polyps in comparison to the normal tissues (RQ>2), which was significantly upper in adenoma polyps compared to the hyperplastic group (P=0.015). Also, unlike the rectum, the AXIN2 gene activity in colon area was higher than normal tissue. |
Conclusion: The results of the current study show that the expression pattern of AXIN2 gene, was markedly changed during the transformation of the normal tissue to polyp. The increased expression level of this gene could be applied as a diagnostic marker in dissociation of the adenoma polyps from hyperplastic ones. On the other hand, the location of the polyps modulates the AXIN2 gene function. Taking together, evaluating the changes of AXIN2, has a precise diagnostic value in the CRC related studies.
Fariba Behnamfar , Matina Jafari , Masoud Moslehi ,
Volume 75, Issue 8 (11-2017)
Volume 75, Issue 8 (11-2017)
Abstract
Background: Endometrial cancer (EC) is the most prevalent genital related cancer of females. One of the controversial points about endometrial cancer surgery is preserving or dissection of sentinel lymph nodes (SLNs). Lymphatic mapping and sentinel nodes sample has been used widely for diverse solid tumors in order of finding metastasis in lymph nodes. The aim of current study was to evaluate diagnostic value of technetium-99 and methylene blue in diagnosis of sentinel lymph node involvement in low-risk endometrial cancer.
Methods: This cross-sectional study was conducted through 2016 on 14 patients with low-grade endometrial cancer referred to Al-Zahra and Shahid Beheshti Hospitals (affiliated to Isfahan University of Medical Sciences), Iran, in 2016-17. Eighteen and twenty-four hours before operation, patients underwent technetium-99 (Tc-99) injection to uterine cervix. Twenty-four hours prior to surgery, patients were referred to resident of gynecology and filled demographic checklist. In next day during operation, Tc-99 was detected by gamma probe. Methylene blue was injected in operation room and blue nodes were detected by naked eye. All patients underwent total hysterectomy, bilateral salpingo-oophorectomy and pelvic lymphadenectomy. Dissected lymph nodes were sent for frozen section and assessment of positive/negative metastasis. Then data were analyzed with SPSS software, version 20 (SPSS Inc., Chicago, IL, USA).
Results: Mean age of our patients was 60.64±9.18 years. Total number of 80 SLNs was dissected. 18.8% of nodes were detected using methylene blue, 12.5% using tecnethium-99 and 6.3% were in common with both methods. Number of two nodes was metastatic and was detected by blue dye and Tc-99. Sensitivity, negative predictive value and detection rate of Tc-99 alone, methylene blue alone and their combination was 100% and false negativity of all above was 100%.
Conclusion: Due to findings of our study, as sensitivity, detection rate, negative predictive value and false negativity of methods lonely and in combination were similar thus based on higher probability of blue dye adverse effects, use of Tc-99 lonely may be adequate.
Methods: This cross-sectional study was conducted through 2016 on 14 patients with low-grade endometrial cancer referred to Al-Zahra and Shahid Beheshti Hospitals (affiliated to Isfahan University of Medical Sciences), Iran, in 2016-17. Eighteen and twenty-four hours before operation, patients underwent technetium-99 (Tc-99) injection to uterine cervix. Twenty-four hours prior to surgery, patients were referred to resident of gynecology and filled demographic checklist. In next day during operation, Tc-99 was detected by gamma probe. Methylene blue was injected in operation room and blue nodes were detected by naked eye. All patients underwent total hysterectomy, bilateral salpingo-oophorectomy and pelvic lymphadenectomy. Dissected lymph nodes were sent for frozen section and assessment of positive/negative metastasis. Then data were analyzed with SPSS software, version 20 (SPSS Inc., Chicago, IL, USA).
Results: Mean age of our patients was 60.64±9.18 years. Total number of 80 SLNs was dissected. 18.8% of nodes were detected using methylene blue, 12.5% using tecnethium-99 and 6.3% were in common with both methods. Number of two nodes was metastatic and was detected by blue dye and Tc-99. Sensitivity, negative predictive value and detection rate of Tc-99 alone, methylene blue alone and their combination was 100% and false negativity of all above was 100%.
Conclusion: Due to findings of our study, as sensitivity, detection rate, negative predictive value and false negativity of methods lonely and in combination were similar thus based on higher probability of blue dye adverse effects, use of Tc-99 lonely may be adequate.
Sajad Shafai , Elham Moslemi , Mehdi Mohammadi , Kasra Esfahani , Amir Izadi ,
Volume 75, Issue 10 (1-2018)
Volume 75, Issue 10 (1-2018)
Abstract
Background: Prostate cancer is one of the most common diseases that affect men. Although prostate cancer is not the fatal flaw in most cases, detection of effective factors for early diagnosis and treatment is essential. Research results have shown that the use of KLK2 plus PSA can be a good biomarker for diagnosing prostate cancer. During prostate cancer, expression of KLK2 gene increases which can be used as a prostate cancer biomarker. The aim of this study is an assessment of KLK2 gene expression as a potential factor in the prostate cancer diagnosis.
Methods: In this case study, 50 prostate cancer urine samples from patients and 50 urine samples from normal individuals who were referred to Mehr Hospital of Tehran (from December 2014 to February 2016) were obtained and stored in the central research laboratory of Shahid Beheshti University of Medical Sciences, Tehran, till tests were being done. The age of collected samples between the 46 up to 71 years. RNA of samples were extracted, and then cDNA was synthesized by using M-MuLV enzyme, Oligo dt, and Random hexamer primers. KLK2 specific primers designed by Primer Express software, version 3.0 (Applied Biosystems, Foster City, CA, USA), and KLK2 gene expression evaluated by using ∆∆ct methods.
Results: In comparison with patients and normal sample`s gene expression, the mean increase expression of KLK2 gene in patients less than 50 years was 2.32 and in patients more than 50 years, it was 5.79, P<0.0001. In addition, gene expression results with respect to GS (Gleason grading system) classification shown that patients with GS6 had the lowest gene expression (3.40) and in the patients with GS8, had the highest gene expression (10.74) in comparison with normal group (P<0.0001).
Conclusion: The expression of KLK2 gene in people with prostate cancer is the higher than the healthy person; finally, according to the results, it could be mentioned that the KLK2 gene considered as a useful factor in prostate cancer, whose expression is associated with progression and development of the prostate cancer.
Methods: In this case study, 50 prostate cancer urine samples from patients and 50 urine samples from normal individuals who were referred to Mehr Hospital of Tehran (from December 2014 to February 2016) were obtained and stored in the central research laboratory of Shahid Beheshti University of Medical Sciences, Tehran, till tests were being done. The age of collected samples between the 46 up to 71 years. RNA of samples were extracted, and then cDNA was synthesized by using M-MuLV enzyme, Oligo dt, and Random hexamer primers. KLK2 specific primers designed by Primer Express software, version 3.0 (Applied Biosystems, Foster City, CA, USA), and KLK2 gene expression evaluated by using ∆∆ct methods.
Results: In comparison with patients and normal sample`s gene expression, the mean increase expression of KLK2 gene in patients less than 50 years was 2.32 and in patients more than 50 years, it was 5.79, P<0.0001. In addition, gene expression results with respect to GS (Gleason grading system) classification shown that patients with GS6 had the lowest gene expression (3.40) and in the patients with GS8, had the highest gene expression (10.74) in comparison with normal group (P<0.0001).
Conclusion: The expression of KLK2 gene in people with prostate cancer is the higher than the healthy person; finally, according to the results, it could be mentioned that the KLK2 gene considered as a useful factor in prostate cancer, whose expression is associated with progression and development of the prostate cancer.
Akram Pourshams, Bahram Kazemi , Sima Kalantari ,
Volume 75, Issue 11 (2-2018)
Volume 75, Issue 11 (2-2018)
Abstract
Cancer is the major cause of death in the world and the rate of mortality is higher in developed countries. Therefore, lifestyle could be effective in promoting the cancer. The pancreatic tumors, are 8th cause of mortality due to cancer, which have several types, among them ductal adenocarcinoma is the most common and includes 85% of cases. Since, it is almost impossible to diagnosis the tumor in early stages of the disease, it contributes to high rates of mortality, although if it diagnosis in early stage and the surgery performed for them only 10-20% of patients will be survived. Metastasis occurs when the tumor is smaller than 2 cm in size and because the pancreas is located in the depth of abdomen, typically, it happens after tumor is spread to other organs. A combination of medical imaging, blood tests, and examination of tissue samples are usually made for diagnosis and based on the cancer stage, surgery, radiotherapy and chemotherapy are chosen as treatment options. Some rare genetic variations can cause pancreatic cancer and about 5-10% of cases are linked to inherited genes. However, major risk factors are including age, obesity, tobacco smoking and diabetes. Smoking counts for about 25% of cases, and the diabetes is the main symptoms of pancreatic cancer, which observed in about 80% of cases. But, it is still unclear whether diabetes is a predisposing factor in pancreatic cancer, or the outcome of tumor progression. Recent studies have shown that, diabetes is unique in pancreatic cancer which is not related to common types. Currently, CA 19-9 is the only reliable tumor marker for pancreatic cancer that its frequency also increases in non-bad conditions, such as pancreatitis and obstructive jaundice, so is not sensitive and specific enough for diagnosis of this cancer. Due to researches continue to find more specific markers. In this review the etiology of pancreatic cancer, diabetes associated with this type of cancer and significant biomarkers for diagnosis will be considered.
Elham Shakiba , Monireh Movahedi , Ahmad Majd , Mehdi Hedayati ,
Volume 75, Issue 12 (3-2018)
Volume 75, Issue 12 (3-2018)
Abstract
Thyroid cancer is one of the most common endocrine malignancies and in the last two decades the number of involved people in the world has been increased. Thyroid cancer in Iran is the seventh most common cancer in women and 14th in men. In recent years many achievements regarding to molecular pathogenic factors such as the substantial role of signaling pathways and molecular abnormalities have been made. Nowadays there is no efficient treatment for progressed thyroid cancer that does not respond to radioiodine therapy which are included poorly differentiated, anaplastic and metastatic or recurrent differentiated thyroid cancer. Although the results of some clinical trials in phase II for treatment of progressed thyroid cancer are rewarding but none of the treated patients responded to treatment and only a few of them responded partially to the treatment which indicates that the treatment can only control the condition of patients with advanced disease, therefore it is needed to consider other alternative solutions which would be helpful in controlling the disease. Epigenetic is referred to study of heritable changes in gene expression without changes in primary DNA sequence. The main mechanisms of genetic and epigenetic alterations are including mutations, increasing the gene copy number and aberrant gene methylation. Epigenetic defects are prevalent in different types of cancers. Aberrant methylation of genes that control cell proliferation and invasion (p16INK4A, RASSF1A, PTEN, Rap1GAP, TIMP3, DAPK, RARβ2, E-cadherin, and CITED1), as well as specific genes involved in differentiation of thyroid cancer (Na+/I- symport, TSH receptor, pendrin, SL5A8, and TTF-1) in association with genetic alterations, leads to tumor progression. Growing evidence shows that acquired epigenetic abnormalities participate with genetic alterations to cause altered patterns of gene expression or function. Many of these molecular changes can be used as molecular markers for prognosis, diagnosis and new therapeutic targets for thyroid cancer. This article is about the most common genetic and epigenetic alterations in thyroid cancer which can be complementary together in recognition of new treatments for the disease.
Sirous Naeimi,
Volume 75, Issue 12 (3-2018)
Volume 75, Issue 12 (3-2018)
Abstract
Background: The main causes and difficulties of cancer are the imbalance between cell growth and cell death. This event is the results of changes in the expression level of genes related to these mechanisms. Among genes including in this case, death-associated protein kinase (DAPK) can be mentioned. Studies have shown that the expression of genes is influenced by the methylation of promoter regions. The purpose of this research was to evaluate the expression of the mentioned gene and the effect of methylation on the expression of this gene and its relationship with developing breast cancer in women.
Methods: Eighty patients with breast cancer and 80 healthy individuals participated in this case-control study which has been referred to Shahid Faghihi and Namazi hospitals, Shiraz city, from August 2014 to March 2017. This study was carried out at the Genetic Research Center of Islamic Azad University, Kazerun Branch, Iran. Peripheral blood lymphocytes were lysed and the mRNAs were extracted using the InViSorb™ RNA preparation kit II (Cat#1062100300, Invitek GmbH, Berlin, Germany) and cleaned up with Qiagen RNeasy spin columns. The first-strand cDNA was synthesized affording to the high capacity cDNA reverse transcription kit procedure. For DAPK gene expression, (Thermo Fisher Scientific, Waltham, MA, USA) PCR technique combines the quantitative performance of SYBR® Green-based real-time PCR, used. This technique is gainful, easy-to-use, and emphases only on the genes that you want. We designated 18S-rRNA gene, as our house-keeping gene. For determine of methylation, methylation-specific polymerase chain reaction (MS-PCR) method was used.
Results: The achieved results from this research show that the levels of DAPK gene expression have a significant difference. The rate of expression in patients was significantly reduced compared with the control group (P=0.0156). Also, the relationship between expression of DAPK factor and lymph node involvement was investigated. The results show the relationship between the factors studied. On the other hand, there was no significant relationship between the expression level of this gene and its promoter methylation (P=0.13).
Conclusion: This research shows that reduction in the rate of DAPK gene expression plays an effective role in the patients with breast cancer.
Methods: Eighty patients with breast cancer and 80 healthy individuals participated in this case-control study which has been referred to Shahid Faghihi and Namazi hospitals, Shiraz city, from August 2014 to March 2017. This study was carried out at the Genetic Research Center of Islamic Azad University, Kazerun Branch, Iran. Peripheral blood lymphocytes were lysed and the mRNAs were extracted using the InViSorb™ RNA preparation kit II (Cat#1062100300, Invitek GmbH, Berlin, Germany) and cleaned up with Qiagen RNeasy spin columns. The first-strand cDNA was synthesized affording to the high capacity cDNA reverse transcription kit procedure. For DAPK gene expression, (Thermo Fisher Scientific, Waltham, MA, USA) PCR technique combines the quantitative performance of SYBR® Green-based real-time PCR, used. This technique is gainful, easy-to-use, and emphases only on the genes that you want. We designated 18S-rRNA gene, as our house-keeping gene. For determine of methylation, methylation-specific polymerase chain reaction (MS-PCR) method was used.
Results: The achieved results from this research show that the levels of DAPK gene expression have a significant difference. The rate of expression in patients was significantly reduced compared with the control group (P=0.0156). Also, the relationship between expression of DAPK factor and lymph node involvement was investigated. The results show the relationship between the factors studied. On the other hand, there was no significant relationship between the expression level of this gene and its promoter methylation (P=0.13).
Conclusion: This research shows that reduction in the rate of DAPK gene expression plays an effective role in the patients with breast cancer.
Arash Salmaninejad , Zahra Golchehre , Mohammad Bagher Eskandari , Eskandar Taghizadeh , Abbas Shakoori ,
Volume 76, Issue 1 (4-2018)
Volume 76, Issue 1 (4-2018)
Abstract
Cancer/testis antigens (CTAs) are a kind of antigens that their expression mostly is restricted in testis and female’s genital organs. Tumor cells often express antigens whose expression is normally limited to germ cells. CTAs are composed of a vast gene family of closely related members and are commonly classified into two groups: the CT-X antigens that are encoded by the X chromosome and the non-X CTAs that are encoded by the autosomes. CTA are extensively and variably dispersed between tumors of diverse histotypes. CTA are broadly expressed in tumors, but not in normal tissue except for testis that is not available to the immune system, actually, the blood-testis barrier and the lack of HLA class I expression on the surface of germ cells avoid the immune system from the interaction with CTA proteins to be identified as non-self-structures. Consequently, CTA can be regarded as fundamentally tumor-specific targets. With extensive investigations on the function of this important biological molecules, their functions are somewhat revealed. Because of their high immunogenicity, tumor-limited, and biased expression, detection of these molecules provides unprecedented chances for further research and clinical development in the field of immunotherapy and cancer diagnosis. Also, growing evidence discloses that a number of CTAs stimulate epithelial mesenchymal transition (EMT) and generation of cancer stem-like cells, increasing metastasis, invasion and tumorigenesis. According to recent clinical attention, more features of CTA regulation are explored. CTA expression has been confirmed in a variety of human cancer tissues and some of them have been discovered to cause humoral and/or cellular immune responses in cancer patients, likewise, they displayed intertumor and intratumor heterogeneity in expression levels. CTAs are excellent targets for targeted tumor therapy, anticancer drug discovery, and diagnostic biomarkers, similarly, appreciated genes in the study of promoting tumorigenesis, immunotherapy, and malignant progression. This review summaries and classifies our current understanding of the complex and biased process of CTAs mRNA and protein expression in cancer, and provide the most current information on their function and regulation.
Saber Soltani , Abolfazl Davoodabadi, Abbas Farahani, Mahsa Dastranj , Masomeh Amini , Navid Momenifar , Shirin Poorabdi , Hojat Veisi ,
Volume 76, Issue 1 (4-2018)
Volume 76, Issue 1 (4-2018)
Abstract
Immunotoxins such as pseudomonas exotoxin are Molecules with a unique structure like toxin-antibody part. These immunotoxins are two functional which crossing the cell membrane and enters the target cell and destroy the cell. Toxin-based treatments are a widespread research field and can have broad applications in the biology and public health. Immunotoxins act selectively against cancer cells and have a good potential for detecting and targeting cancer cells. Specific immunotoxins to target immune cells due to the selection type antibody and antibodies are responsible for the identification of the target cells. Cancer is becoming a major cause of death in most developed countries. In order to have a strong factor in cancer repression, that agent must target the cancer cells directly and specifically. Often, but not always, immunotoxins are produced for disabling and killing cancer cells, that this issue is one of new therapeutic approaches in recently. Clinical aims to designing and create new cancer therapies focused with this approach, a lot of information about the toxin and intracellular pathways have been obtained. So, toxins in medicine are useful for the treatment of human disease and study of professional cellular functions. So, immunotoxins have a high potential for cancer treatment. Other applications of immunotoxins, including immune system regulation and treatment of viral diseases and parasites diseases. More research is needed to improve the immunotoxin effects and to reduce their side effects. On the whole, with design creative, clever and experienced programs, many human diseases, particularly cancers can be in a short period of time and faster than other methods of treatment that the treatment of long, to be treated. Following the design and implementation of clinical trials, the effects of immunotoxins on animal tumorigenic models were performed. In fact, in this study, we focus on the use of protein-bound toxins with bacterial and herbal sources and more specifically Pseudomonas immunotoxins which attached to antibodies to target cancer cells.
Seyedeh Hakimeh Rezazadeh, Reza Shirkoohi, Abdolhamid Angaji, Seyed Yusef Seyedena, Amir Nader Emami Razavi,
Volume 76, Issue 2 (5-2018)
Volume 76, Issue 2 (5-2018)
Abstract
Background: Ovarian cancer is a leading metastatic disease. The epithelial ovarian cancer is one of the most common malignant cancers that usually remains asymptomatic up to metastasis stages, and most patient when diagnosed are in the advanced stage of the disease. Studies have shown that in the majority of epithelial cancers mesenchymal factor expression such as Vimentin increases, and the epithelial factor expression such as E-cadherin decreases, as a result, it causes an epithelial-mesenchymal transition (EMT). The aim of this study was to determine the expression level of these genes and association between EMT phenomenon and development of ovarian cancer based on clinical and morphological findings.
Methods: In the present case series study, 70 samples were chosen from the tumor Bank of Cancer Institute taken from patients at Imam Khomeini Hospital, Tehran, Iran. The amount of expression of two genes, E-cadherin and vimentin, was investigated by real-time PCR method from February 2016 to September 2017. The RNA extraction was done manually, and then cDNA synthesis was performed; In each sample the expression level of vimentin and E-cadherin was measured with real-time PCR method. The patient’s clinical information with other data were analyzed with nonparametric statistical methods in SPSS software, version 19 (SPSS Inc., Chicago, IL, USA).
Results: There was a significant relationship between expression of vimentin gene and the stage (P=0.026) of the disease and metastasis (P=0.009), There was no significant relationship between vimentin gene expression and tumor grade (P=0.207), age (P=0.11), tumor size (P=0.71) and family history (P=0.6). There was a significant correlation between E-cadherin gene expression and metastasis (P=0.027), no significant correlation was found between E-cadherin gene expression with tumor grade (P=0.690), stage (P=0.753), age (P=0.09), tumor size (P=0.537) and family history (P=0.56).
Conclusion: According to the changes in expression of vimentin and E-cadherin genes in ovarian tumor cells, and association between these two genes with clinical and morphological findings and the role of these genes in the migration and invasion, we can use the both genes, vimentin and E-cadherin, as genes involved in the EMT process to assess disease progression and incidence of cell invasion in ovarian cancer.
Methods: In the present case series study, 70 samples were chosen from the tumor Bank of Cancer Institute taken from patients at Imam Khomeini Hospital, Tehran, Iran. The amount of expression of two genes, E-cadherin and vimentin, was investigated by real-time PCR method from February 2016 to September 2017. The RNA extraction was done manually, and then cDNA synthesis was performed; In each sample the expression level of vimentin and E-cadherin was measured with real-time PCR method. The patient’s clinical information with other data were analyzed with nonparametric statistical methods in SPSS software, version 19 (SPSS Inc., Chicago, IL, USA).
Results: There was a significant relationship between expression of vimentin gene and the stage (P=0.026) of the disease and metastasis (P=0.009), There was no significant relationship between vimentin gene expression and tumor grade (P=0.207), age (P=0.11), tumor size (P=0.71) and family history (P=0.6). There was a significant correlation between E-cadherin gene expression and metastasis (P=0.027), no significant correlation was found between E-cadherin gene expression with tumor grade (P=0.690), stage (P=0.753), age (P=0.09), tumor size (P=0.537) and family history (P=0.56).
Conclusion: According to the changes in expression of vimentin and E-cadherin genes in ovarian tumor cells, and association between these two genes with clinical and morphological findings and the role of these genes in the migration and invasion, we can use the both genes, vimentin and E-cadherin, as genes involved in the EMT process to assess disease progression and incidence of cell invasion in ovarian cancer.
Fateme Sadat Kia , Ehsan Nazemalhosseini-Mojarad, Flora Forouzesh,
Volume 76, Issue 2 (5-2018)
Volume 76, Issue 2 (5-2018)
Abstract
Background: Most of colorectal cancers arise from intestinal polyps. Evaluating of the expression level of genes that are involved in tumors growth and development, may consider as diagnostic factor of malignancy in the polyps. Failure of apoptosis is one of the causes of cancers. One of the key molecules in this pathway is Bid gene which connects the extrinsic to the intrinsic apoptosis pathways. The aim of this study was to investigate the quantitative expression of Bid gene in colorectal adenomatous polyps compared to control group.
Methods: The investigated population was chosen from the cases with colonic polyps that referred to the Taleghani Hospital, Tehran, Iran, from April 2014 to May 2016. 22 biopsy samples from patients with adenomatous polyps and 10 samples from healthy individuals as control group were selected. Demographic and clinical properties were collected from patients' files. The Bid gene expression was evaluated using Real-time PCR by ABI 7500 (Applied Biosystems Inc., Foster City, CA, USA). Results were analyzed by the ABI 7500 system SDS version 2.3 and GraphPad Prism, version 5 (GraphPad Software Inc., La Jolla, CA, USA). the expression changes of the intended gene in target groups were compared with the normal tissues using the 2-∆∆CT equation.
Results: Based on the quantitative real-time PCR, the gene expression of Bid gene significantly increased in adenomatous polyps in comparison with the control group (healthy individuals) (RQ>2). Also, polyps were seen in ascending colon, transverse colon, descending colon and rectum showed increased expression compared to control group, but in the sigmoid section of the intestine, there was no change in expression of Bid gene compared to control group.
Conclusion: According to the present study, the expression of Bid gene increased in adenomatous polyps, compared with the normal tissue (healthy group). It suggests that Bid gene by increasing the expression in response to the onset of dysplasia and disruption of the apoptotic cycle, it tries to compensate for the apoptosis.
Methods: The investigated population was chosen from the cases with colonic polyps that referred to the Taleghani Hospital, Tehran, Iran, from April 2014 to May 2016. 22 biopsy samples from patients with adenomatous polyps and 10 samples from healthy individuals as control group were selected. Demographic and clinical properties were collected from patients' files. The Bid gene expression was evaluated using Real-time PCR by ABI 7500 (Applied Biosystems Inc., Foster City, CA, USA). Results were analyzed by the ABI 7500 system SDS version 2.3 and GraphPad Prism, version 5 (GraphPad Software Inc., La Jolla, CA, USA). the expression changes of the intended gene in target groups were compared with the normal tissues using the 2-∆∆CT equation.
Results: Based on the quantitative real-time PCR, the gene expression of Bid gene significantly increased in adenomatous polyps in comparison with the control group (healthy individuals) (RQ>2). Also, polyps were seen in ascending colon, transverse colon, descending colon and rectum showed increased expression compared to control group, but in the sigmoid section of the intestine, there was no change in expression of Bid gene compared to control group.
Conclusion: According to the present study, the expression of Bid gene increased in adenomatous polyps, compared with the normal tissue (healthy group). It suggests that Bid gene by increasing the expression in response to the onset of dysplasia and disruption of the apoptotic cycle, it tries to compensate for the apoptosis.
Roghayeh Larki, Leila Rouhi , Seyed Hossein Hejazi ,
Volume 76, Issue 3 (6-2018)
Volume 76, Issue 3 (6-2018)
Abstract
Background: Breast cancer is a malignant proliferation of epithelial cells that lining the ducts or lobules of the breast. Breast cancer is the second common cancer (after lung cancer) in women. Gallic acid, being a polyphenols, has been reported for its antiproliferative activity against many cancer cell lines. Objective of the present study is effect of gallic acid on proliferation and apoptosis of the human breast adenocarcinoma cell lines SKBR3 and normal fibroblasts cells.
Methods: This experimental study was performed in cellular and developmental biology of Shahrekord Islamic Azad University, Iran from April to August 2015. For anti-cancer activity, in this study SKBR3 cells and normal fibroblast cells (HU-02) were cultured in Dulbecco's modified eagle's medium, DMEM (Gibco, Life Technologies, Inc., New York, USA) medium with 10% fetal bovine serum, FBS (Gibco, Life Technologies, Inc., New York, USA). The SKBR3 and normal fibroblast cells were treated in the medium of DMEM medium and gallic acid (20, 40, 80, 100 and 200 µg/ml) for 24, 48 and 72 hours. Cells viability was assessed by MTS (Methyl- Thiazol-) assay. Cells were seeded at 5×103 cells/ml in 96 well plates and incubated for 24 hours. Then metabolites of bacteria were added, after indicated times MTS (20µl) was added and the absorbance was measured at 492 nm using ELISA plate reader. The percentage of apoptosis induction was determined by flow cytometry analysis using Annexin-V fluorescein isothiocyanate (FITC) kit (BioVision Products, CA, USA) in 20, 40, 80, 100 and 200 µg/ml concentration of gallic acid at 48 hours incubation.
Results: Gallic acid decreases significantly the viability of SKBR3 cell line in a time and dose dependent manner. So that the most effective concentration of this substance was 200 µg/ml and 72 hours after treatment (P< 0.05). According to the data of Annexin-PI, the highest apoptosis induction rate was seen in 200 µg/ml (P< 0.05). While gallic acid in various concentrations had no significant effect on normal fibroblast cells.
Conclusion: Objective of the present study is effect of gallic acid on proliferation and apoptosis of the human breast adenocarcinoma cell lines SKBR3 and normal fibroblasts cells.
Methods: This experimental study was performed in cellular and developmental biology of Shahrekord Islamic Azad University, Iran from April to August 2015. For anti-cancer activity, in this study SKBR3 cells and normal fibroblast cells (HU-02) were cultured in Dulbecco's modified eagle's medium, DMEM (Gibco, Life Technologies, Inc., New York, USA) medium with 10% fetal bovine serum, FBS (Gibco, Life Technologies, Inc., New York, USA). The SKBR3 and normal fibroblast cells were treated in the medium of DMEM medium and gallic acid (20, 40, 80, 100 and 200 µg/ml) for 24, 48 and 72 hours. Cells viability was assessed by MTS (Methyl- Thiazol-) assay. Cells were seeded at 5×103 cells/ml in 96 well plates and incubated for 24 hours. Then metabolites of bacteria were added, after indicated times MTS (20µl) was added and the absorbance was measured at 492 nm using ELISA plate reader. The percentage of apoptosis induction was determined by flow cytometry analysis using Annexin-V fluorescein isothiocyanate (FITC) kit (BioVision Products, CA, USA) in 20, 40, 80, 100 and 200 µg/ml concentration of gallic acid at 48 hours incubation.
Results: Gallic acid decreases significantly the viability of SKBR3 cell line in a time and dose dependent manner. So that the most effective concentration of this substance was 200 µg/ml and 72 hours after treatment (P< 0.05). According to the data of Annexin-PI, the highest apoptosis induction rate was seen in 200 µg/ml (P< 0.05). While gallic acid in various concentrations had no significant effect on normal fibroblast cells.
Conclusion: Objective of the present study is effect of gallic acid on proliferation and apoptosis of the human breast adenocarcinoma cell lines SKBR3 and normal fibroblasts cells.
Mohammadreza Noori-Daloii , Bahareh Kashani ,
Volume 76, Issue 4 (7-2018)
Volume 76, Issue 4 (7-2018)
Abstract
Cancer is one of the most dangerous health problems of today modern societies which has an increasing rate especially in developing countries. There are many diverse ongoing treatment attempts trying to defeat cancer. Despite that, scientists have been unable to find a permanent cure for this disease. In many cases although there is a successful first response in patients, cancer cells are finally able to withstand therapeutic procedures and even use chemo-resistance to take advantage of treatments to facilitate tumor growth, resulting in cancer remission. Therefore, and mostly in recent two decades, scientists have been trying to choose their treatments just as smart to be able to conquer cancer. One of the best methods of this smart defense is to target weak points of neoplastic cells and use them for designing drugs. In this case it would be most probable for cancer cells not to have a chance to confront and cause chemo-resistance. Total endeavors to fulfill this goal are named “targeted cancer therapy”. This therapeutic approach is mostly consisted of two different procedures: 1- designing and using specific drugs to target cancer cells’ mutated genes; which will be defined by checking the genetic background of tumor cells for each specific cancer type. EGFR, RAS, VEGF and HIF-1α are among the pathways that have already been used as targets. 2- The other procedure could be methods that would carry drugs directly to unhealthy cells to prevent further side effects for normal cells of patients. It would be possible by designing specific antibodies to target antigens of neoplastic cells. Ribonucleic sequences (miRNAs and siRNAs) are also very promising as new drugs and nanoparticles have enabled us to increase drug concentration in tumors. The ultimate goal of these new experiments is to suggest specific drugs for each patient based on the nature of one's disease and genetic background, which will bring about "personalized medicine" era. Using valid new references, this review article first presents targets that are currently being used for this targeted therapy, their logic of choice and the drugs that have already been produced for clinical trials. Smart methods of drug delivery are also presented and discussed afterwards.
Sima Kadkhodayan , Asieh Maleki , Malihe Hasanzadeh , Zohreh Yousefi,
Volume 76, Issue 5 (8-2018)
Volume 76, Issue 5 (8-2018)
Abstract
Background: Cancer of the endometrium is the most common gynecologic malignancy in western and industrial countries, and is the second most common in developing countries, therefore it is of special importance. Adenocarcinoma of the endometrium is the most common type of uterine cancer. The prevalence of endometrial cancer in young women under the age of 40 in western country is very low and about 5 percent. The aim of this study was to determine the prevalence of endometrial cancer at age ≤40 years in our center during 4 years.
Methods: In a cross-sectional study, all medical records of patients with endometrial cancer in Ghaem University Hospital, Mashhad, Iran was reviewed to identify women <40 years of age with endometrial cancer, over the course of 4 years, (from 2012 to 2015). The risk factors for endometrial cancer, such as obesity, polycystic ovary syndrome (PCO), infertility, and a history of cancer in the family or individual, were collected in each patient. Clinical features, histological type of endometrial carcinoma, and therapeutic action also were gathered.
Results: A total of 119 patients with endometrial cancer that was admitted in our genecology oncology center were evaluated. 19 patients (15.9%) were younger than 40 years old. 16 cases (84.2%) with endometrial adenocarcinoma and 3 (15.7%) had endometrial stromal sarcoma. The youngest patient was 27 years old and the oldest was 39 years. Seven patients (8/36%) had infertility and we don’t know about fertility condition in 3, because they were single. 12 cases (63%) were overweight (BMI≥35) and 6 cases (5/31%) had polycystic ovarian disease (PCOD). In 2 patients, there was concomitant ovarian and endometrial cancer. Histology report of both ovaries was endometrioid and both patients were overweight. Obesity, poly cystic ovary syndrome (PCOD) and Infertility were the most important risk factors for endometrial cancer in young patients.
Conclusion: The prevalence of endometrial cancer in young women under the age of 40 in our country is so higher than the statistics provided in industrial countries.
Methods: In a cross-sectional study, all medical records of patients with endometrial cancer in Ghaem University Hospital, Mashhad, Iran was reviewed to identify women <40 years of age with endometrial cancer, over the course of 4 years, (from 2012 to 2015). The risk factors for endometrial cancer, such as obesity, polycystic ovary syndrome (PCO), infertility, and a history of cancer in the family or individual, were collected in each patient. Clinical features, histological type of endometrial carcinoma, and therapeutic action also were gathered.
Results: A total of 119 patients with endometrial cancer that was admitted in our genecology oncology center were evaluated. 19 patients (15.9%) were younger than 40 years old. 16 cases (84.2%) with endometrial adenocarcinoma and 3 (15.7%) had endometrial stromal sarcoma. The youngest patient was 27 years old and the oldest was 39 years. Seven patients (8/36%) had infertility and we don’t know about fertility condition in 3, because they were single. 12 cases (63%) were overweight (BMI≥35) and 6 cases (5/31%) had polycystic ovarian disease (PCOD). In 2 patients, there was concomitant ovarian and endometrial cancer. Histology report of both ovaries was endometrioid and both patients were overweight. Obesity, poly cystic ovary syndrome (PCOD) and Infertility were the most important risk factors for endometrial cancer in young patients.
Conclusion: The prevalence of endometrial cancer in young women under the age of 40 in our country is so higher than the statistics provided in industrial countries.
Esmat Abdi , Saeid Latifi-Navid , Hamid Latifi-Navid , Saber Zahri, Abbas Yazdanbod ,
Volume 76, Issue 6 (9-2018)
Volume 76, Issue 6 (9-2018)
Abstract
Gastric cancer (GC) is the second leading cause of cancer-related deaths worldwide. It has been proposed that the specific genotypes of Helicobacter pylori (H. pylori) are the causative agents in the development of gastroduodenal diseases, such as chronic atrophic gastritis, peptic ulcerations, and GC. However, disease progression to GC occurs in only a small proportion of infected patients. Recently, we identified a novel polymorphic site in the 3ʹ-end region of H. pylori vacA gene. The vacA c1 genotype increased the risk of GC. This association was independent of and larger than the associations of the m-, i-, and d-type of vacA or cagA status with GC. Therefore, treatment of H. pylori infection may be an effective way to prevent GC. Expression of cytokines and their associations with inflammatory responses has been shown. Several cytokine polymorphisms, such as IL-1B, IL-8, IL-10, and TNF-α have been considered as risk factors for GC. It has been shown that the interaction of bacterial genotypes and host factors plays an essential role in developing GC. Several altered molecular pathways are involved in the pathogenesis of GC. Micro-RNAs are small, non-coding RNAs of 18-25 nucleotides in length that regulate the expression of target mRNAs. Expression pattern of cancer cells is different compared with the normal cells. Micro-RNAs plays a critical role in apoptosis and classified in two groups: pro- and anti-apoptotic agents. Recent studies have confirmed the oncogenic or tumor suppression role of micro-RNAs in cancer cells. They play a significant role in the GC cell physiology and tumor progression, by translational suppression of target genes. These small RNAs have therefore emerged as a new type of GC biomarker with immeasurable clinical potential. Generally, a variety of micro-RNAs involved in different stages of cancer, including tumorigenesis, angiogenesis, and metastasis. Considering to this issue more than 50% of cancers can be cured, if they were diagnosed in the early stages. Hence, identifying the biomarkers of GC could play an important role in prevention, early diagnosis and rapid treatment of patients. In this review article, we have reviewed the latest findings about bacterial and tissue biomarkers of GC
Fahimeh Kalbkhani , Mohammad Reza Sam ,
Volume 76, Issue 6 (9-2018)
Volume 76, Issue 6 (9-2018)
Abstract
Background: Using natural compounds with low toxicity on normal cells and high efficacy on malignant cells is highly appreciated for treatment of colorectal cancer (CRC). In the present study, the effect of fish-oil derived eicosapentaenoic acid (EPA) on the cell number, cell proliferation rate and caspase-3 enzyme activity in LS174T human colorectal cancer cell line was investigated.
Methods: This experimental study was performed in cell culture lab, Institute of Biotechnology, affiliated to the Urmia University, Urmia, Iran from April to September 2017. LS174T colorectal cancer cells at a density of 5×105 cells per well were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) and kept at 37 °C in a humidified incubator with 5% CO2 for 24 hours. Thereafter, the cells were treated with 50, 100, 150 and 200 μmol EPA for 48 hours and cell numbers were counted using neobauer chamber and caspase-3 activities were measured by performing the caspase-3 colorimetric assay (Abcam, Cambridge, MA, USA). Furthermore, 5×103 LS174T colorectal cancer cells were cultured and treated with the above-mentioned EPA concentrations for 24, 48 and 72 hours, after which cell proliferation rate was evaluated by WST-1 proliferation assay (Roche Diagnostics, Mannheim, Germany).
Results: Treatment of LS174T colorectal cancer cells with 50, 100, 150 and 200 μmol EPA decreased the number of cells in a dose-dependent manner. We also found that treatment of malignant cells with increasing EPA concentrations (50 to 200 μmol) significantly decreased cell proliferation in a dose and time dependent manner. After a 72 hours treatment of LS174T cells with 200 μmol EPA, cell proliferation was calculated to be 30.3% compared to untreated control cells. Following 48 hours treatment, caspase-3 activity increased with increasing EPA concentrations in which at 200 μmol EPA, caspase-3 activity increased by 3.4 fold compared to untreated control cells.
Conclusion: Fish-oil derived eicosapentaenoic acid as a safe compound decreases the number of colorectal cancer cells and their proliferation rate and activates caspase-3 enzyme, as an executor protein in apoptosis.
Methods: This experimental study was performed in cell culture lab, Institute of Biotechnology, affiliated to the Urmia University, Urmia, Iran from April to September 2017. LS174T colorectal cancer cells at a density of 5×105 cells per well were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) and kept at 37 °C in a humidified incubator with 5% CO2 for 24 hours. Thereafter, the cells were treated with 50, 100, 150 and 200 μmol EPA for 48 hours and cell numbers were counted using neobauer chamber and caspase-3 activities were measured by performing the caspase-3 colorimetric assay (Abcam, Cambridge, MA, USA). Furthermore, 5×103 LS174T colorectal cancer cells were cultured and treated with the above-mentioned EPA concentrations for 24, 48 and 72 hours, after which cell proliferation rate was evaluated by WST-1 proliferation assay (Roche Diagnostics, Mannheim, Germany).
Results: Treatment of LS174T colorectal cancer cells with 50, 100, 150 and 200 μmol EPA decreased the number of cells in a dose-dependent manner. We also found that treatment of malignant cells with increasing EPA concentrations (50 to 200 μmol) significantly decreased cell proliferation in a dose and time dependent manner. After a 72 hours treatment of LS174T cells with 200 μmol EPA, cell proliferation was calculated to be 30.3% compared to untreated control cells. Following 48 hours treatment, caspase-3 activity increased with increasing EPA concentrations in which at 200 μmol EPA, caspase-3 activity increased by 3.4 fold compared to untreated control cells.
Conclusion: Fish-oil derived eicosapentaenoic acid as a safe compound decreases the number of colorectal cancer cells and their proliferation rate and activates caspase-3 enzyme, as an executor protein in apoptosis.
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