Micro RNA-34a sensitizes MCF-7 breast cancer cells to carboplatin through the apoptosis induction

Abstract

AimBreast cancer (BC) has been classified among the main causes of death owing to females' cancer. Carboplatin is a platinum-based chemotherapeutic drug that is an important treatment option for BC. But high and frequent doses of carboplatin usually reducing the reaction of cancer cells to medication. There is an immediate need to establish methods for increasing the carboplatin susceptibility to BC cells. For instance, micro RNAs (miRNAs) such as MiR34a demonstrate significant potential. Considering that, this research was planned to explore the better clinical effect and underlying mechanism of miR-34a as a possible tumor inhibitor and drug resistance regulator in compared with carboplatin chemotherapy drug in the cell lines of BC in humans. MethodsMCF-7 cell line was transfected with miR-34a to perform functional analyses. Subsequently, the MTT assay was applied to assess cell viability. Cell viability and cell death-associated gene expression amounts including Bax, Bcl-2, caspase-3, MDR1, P53, and mir34-a, were examined through quantitative real-time PCR. ResultsFindings showed that miR-34a upregulation significantly decreased MCF7 cell viability in comparison with the control group. Furthermore, the single treatment of cells with miR-34a mimics and carboplatin could significantly increase Bax, Caspase-3, P53, and decrease in Bcl-2 mRNA expression levels compared to the non-treated group. Moreover, by reducing the expression levels of the MDR1 gene, BC cells' reaction to carboplatin has been increased via miR-34a. ConclusionThis study showed, that miR-34a restoration might improve the responsiveness of breast cancer cells to carboplatin chemotherapy through the downregulation of MDR1.