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

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.