Breast cancer (BC) is the leading cause of death in females worldwide. Although
cisplatin is a strong-effect and broad-spectrum
chemotherapy drug, resistance to
cisplatin remains a significant factor effecting clinical efficacy. The underlying mechanism of
cancer cell resistance to
cisplatin is not fully understood.
MicroRNAs (miRs/
miRNAs), as a regulator, are involved in regulating chemosensitivity to numerous chemotherapeutic drugs. The present study aimed to investigate the function of miR-181a-5p as a potential
tumor suppressor in improving the efficiency of
cisplatin in BC. The IC50 of
cisplatin and miR-181a-5p expression were determined in five BC cell lines, and HS578T was selected as an appropriate cell line for subsequent experiments. The sensitivity of HS578T cells to
cisplatin was assessed using cell proliferation, migration and apoptosis assays. Western blotting was performed to detect the expression of
vitamin D receptor (VDR) and autophagy in HS578T cells. It was found that the increase in autophagy resulted in increased apoptosis and sensitivity to
cisplatin in HS578T cells. miR-181a-5p transfection also inhibited the proliferation and migration ability of HS578T cells and induced apoptosis. Meanwhile, HS578T cells have increased sensitivity to
cisplatin. VDR, as a target gene and autophagy regulator of miR-181a-5p, was negatively regulated by miR-181a-5p. Upon the decrease in VDR expression, the autophagy in HS578T cells was increased. These results indicate that the increase in autophagy enhanced the chemosensitivity of
cisplatin by inducing apoptosis of HS578T cells and by inhibiting proliferation and migration. The present study showed that miR-181a-5p increased the chemical sensitivity of HS578T cells to
cisplatin by inhibiting VDR to promote autophagy. The use of miR-181a-5p/autophagy/VDR-based treatment strategies may be a potential method to overcome
cisplatin resistance in BC.