Fatemeh Kaboudan, Soheila Talesh Sasani, Seyed Mohsen Asghari,
Volume 8, Issue 1 (6-2021)
Abstract
Breast cancer is the fourth common cancer worldwide and occurs when breast cells begin to uncontrolled division and tumor formation. Angiogenesis is one of the essential factors in cell growth and maintenance of homeostasis in the natural and pathological conditions, while VEGFs are the most critical factors in angiogenesis. MiR-210 plays an important role in the angiogenesis via association with VEGF. Here, the miR-210 expression changes in response to a VEGFB antagonist peptide, called VEGB1, was studied in female BALB/c mice bearing 4T1 cell line induced breast tumor. The treated group received 1mg.kg-1 and 10mg.kg-1 of the peptide and the control group received PBS intraperitoneally during two weeks. Both of the animal groups underwent a resection of breast tissue 14 days after treatment and miR-210 expression level was investigated. Statistical analysis by On-way ANOVA showed that the expression level of miR-210 gene had significant differences among the groups treated with various doses of VEGB1. Also, the gene expression was significantly different between peptide-treated groups and control samples (p<0.05). MiR-210 expression level had 42% reduction in mice treated with 1mg.kg-1 of VEGB1, while 90% was seen in mice treated with 10mg.kg-1 of VEGB1 showing the inhibitory function of VEGB1 antagonist peptide at different doses.
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.
