Downregulated miR‑130a enhances the sensitivity of acute myeloid leukemia cells to Adriamycin

Abstract

MicroRNA (miR)‑130a has been reported to promote cancer growth; however, its role during acute myeloid leukemia (AML) is not completely understood. In the present study, the effects of miR‑130a on the sensitivity of AML cells to Adriamycin (Adr) were investigated. 5‑Aza‑2'‑deoxycytidine (5‑Aza‑dC) was used to stimulate Adr resistance in AML cells, and cell viability and miR‑130a expression were determined using the Cell Counting Kit‑8 (CCK‑8) assay and reverse transcription‑quantitative PCR, respectively. miR‑130a overexpression and knockdown in Adr‑resistant AML cells was performed to investigate the proliferative and invasive abilities of the cells using CCK‑8 and Transwell assays, respectively. Furthermore, the effects of miR‑130a on the expression of epithelial‑mesenchymal transition (EMT)‑related proteins in Adr‑resistant AML cells were detected using western blot analysis. Pre‑treatment with 5‑Aza‑dC enhanced the cell viability and miR‑130a expression of Adr‑treated AML cells. Adr and miR‑130a expression showed a dose‑dependent relationship, with miR‑130a expression decreasing with increasing Adr concentrations. Moreover, miR‑130a overexpression alleviated the inhibitory effects of Adr on cell viability and invasion, while miR‑130a knockdown enhanced the sensitivity of AML cells to Adr. Furthermore, Adr exerted an inhibitory effect on EMT in AML cells, which was rescued by miR‑130a overexpression and enhanced by miR‑130a knockdown. miR‑130a knockdown also increased the sensitivity of AML cells to Adr by decreasing cell viability, invasion and EMT. Therefore, miR‑130a knockdown is a potential therapeutic strategy for Adr‑resistant AML.