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Showing 2 results for Derakhshan

Elahe Derakhshanfar, Shaban Alizadeh, Hassan Rafiemehr , Fateme Nadali, Ali Qasemi, Masuod Karimi, Nushin Shabab,
Volume 10, Issue 6 (3-2017)
Abstract

Background and Aim: Chronic myeloid leukemia (CML) is a myeloprolifrative neoplasm that is characterized by an expansion of myeloid, erythroid cells and platelets in peripheral blood and myeloid hyperplasia in bone marrow. Secreted frizzled-related protein family is a negative regulator of the Wnt signaling pathway that suppresses this signaling pathway in healthy individuals. Aberrant regulation of the Wnt signaling pathway is a prevalent theme in cancer biology, and methylation in promoter of SFRP family has been shown to cause uncontrolled cell proliferation in cancer. Chronic myeloid leukemia was the first malignancy in which the important role of Wnt signaling pathway has been described. 
In the present study, we examined the methylation status of SFRP1 and SFRP2 genes in patients with CML.
Materials and Methods: Blood samples were obtained from 25 healthy individuals and 33 patients whit chronic meyloied leukemia (23 male, 10 female) Then Isolated DNA was treated with sodium bisulfite and analyzed by methylation-specific polymerase chain reaction (MSP) with primers specific for methylated and unmethylated promoter sequences of the SFRP1 & -2 genes. We used Mann-Whitney u-tests to investigate the correlation between SFRP-1 and SFRP-2 genes hypermethylation and clinical parameters.
Results: In CML patient hypermethyleation frequency of SFRP-1 and SFRP-2 genes were 16.1℅ and 27.2% respectively. In control group SFRP-1 and SFRP-2 genes were unmethylated.
Conclusion: The present study showed that, methylation of SFRP genes also occurs in CML like other solid tumors. Therefore, the methylation of these genes may play a role in the initiation of malignant disease.


Shima Derakhshan, Negar Yavari Tehrani Fard, Nahid Abotalbe, Maryam Naseroleslami,
Volume 17, Issue 2 (5-2023)
Abstract

Background and Aim: Today, natural compounds such as peptides and probiotics can be mentioned as a supplement to the treatment of diseases such as cancer. These compounds may be effective in preventing the progression or treatment of cancer by affecting some molecular pathways including inflammation. The aim of this study was to investigate the effect of D-peptide-B and B.bifidum probiotic lysate on the expression of TNF-α and IL-1 genes in gastric cancer cells of AGS cell line.
Materials and Methods: In this study, AGS and HEK cells were cultured in DMEM medium with 10% bovine serum. The cells were treated with different concentrations of D-peptide-B and B.bifidum lysate and were incubated for 24 hours. The cell viability was checked by MTT. For molecular investigations, after RNA extraction and cDNA synthesis, the relative expression of TNF-α and IL-1 genes was evaluated using Real time PCR, and the data were analyzed using statistical methods One-way ANOVA.
Results: The MTT results indicated that the AGS cancer cells’ survival rate decreased after treatment with dipeptide-B and lysate of B.bifidum as compared to HEK control cells. Furthermore, the study found that the expression levels of TNF-α and IL-1 genes in gastric cancer cells were significantly higher after treatment with D-Peptide-B, bacterial lysate, or both, when compared to normal HEK cells (P≤0.05). Specifically, the IL-1 gene expression increased by 300% (4 times) for peptide treatment, 100% (2 times) for bacterial treatment, and 650% (7.5 times) for combined treatment. Similarly, the TNF-α gene expression increased by 350% for peptide treatment, 100% for bacterial treatment, and 520% for combined treatment. These results suggest that these compounds may have induced cell death in cancer cells by affecting other molecular pathways.
Conclusion: Considering that D-peptide-B and B.bifidum lysate had no significant toxicity on normal cells and caused a significant decrease in the survival of cancer cells and this toxicity was dose dependent, therefore, consideration might be given to these natural compounds in treatment of gastric cancer.


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