Mona Motaharinia, Mohammad Nabiuni,
Volume 8, Issue 4 (1-2022)
Abstract
Lung carcinoma is the second most common type of cancer. Inefficiency of the current treatments and the undesirable side effects of chemotherapy drugs made the know-how of the treatment important. The purpose of this study is to investigate the synergic effect of curcumin and Cisplatin in comparison with the sole application of each treatment on Calu-6 cell line, an epithelial cell line of human lung carcinoma, and the expression of Cdc42 gene. The viability of Calu-6 was examined after 24- or 48-hour treatment with doses of 0.5 to 8 µg/ml of curcumin, 0.1 to 50 µg/ml of cisplatin and combined doses of curcumin and Cisplatin by MTT assay. To measure apoptosis and the expression of Cdc42 gene, flow cytometry and Real-Time PCR were utilized. Decrease of cell viability and induction of cell death were observed in the cells treated with 0.67 µg/ml of curcumin and 1.7 µg/ml of cisplatin (the lowest effective dose) and the combined treatment with the same doses of each drug after 24-hour treatments. The maximum rates of early and late apoptosis were related to treatment with curcumin and the combined treatment. The gene expression analysis results indicated that both Curcumin and Cisplatin decrease the expression of Cdc42 gene, moreover, their co-administration showed synergic effects. Therefore, Curcumin could be an appropriate option for complementary administration with other chemotherapy agents in order to reduce their efficient dose, and to reduce their side effects.
Leila Gholami, Farnoosh Attari, Mahmood Talkhabi, Fatemeh Saadatpour,
Volume 10, Issue 1 (6-2023)
Abstract
Breast cancer is the most common cause of death from cancer among women. The triple-negative breast cancer (TNBC) is the most invasive subtype, and chemotherapy is the only therapy option. Cancer cells preferably utilize the glycolysis pathway even with proper oxygen availability, and this activation plays a great role in tumorigenesis. Therefore, glycolysis targeting can be an effective strategy for cancer treatment. Here, the apoptotic effect of a glycolysis inhibitor named dichloroacetate (DCA) on TNBC cells MDA-MB-231 was assessed, and the expression of anti-apoptotic genes and oncogenic miRNAs was evaluated. MTT assay showed that DCA reduces cell viability in a dose-dependent manner with the IC50 concentration of 50 mM. Annexin/PI assay demonstrated that DCA due to DCA treatment. Finally, the expression of anti-apoptotic genes Bcl2l1 and Mcl1 and oncogenic miRNAs miR21 and miR27a decreased due to DCA treatment. Our results confirmed that DCA, as a glycolysis inhibitor, leads to apoptosis induction in TNBC cells because of reducing expression of viability genes and miRNAs.
