Downregulated miR­130a 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 miR­130a on the sensitivity of AML cells to Adriamycin (Adr) were investigated. 5­Aza­2'­deoxycytidine (5­Aza­dC) was used to stimulate Adr resistance in AML cells, and cell viability and miR­130a expression were determined using the Cell Counting Kit­8 (CCK­8) assay and reverse transcription­quantitative PCR, respectively. miR­130a overexpression and knockdown in Adr­resistant AML cells was performed to investigate the proliferative and invasive abilities of the cells using CCK­8 and Transwell assays, respectively. Furthermore, the effects of miR­130a on the expression of epithelial­mesenchymal transition (EMT)­related proteins in Adr­resistant AML cells were detected using western blot analysis. Pre­treatment with 5­Aza­dC enhanced the cell viability and miR­130a expression of Adr­treated AML cells. Adr and miR­130a expression showed a dose­dependent relationship, with miR­130a expression decreasing with increasing Adr concentrations. Moreover, miR­130a overexpression alleviated the inhibitory effects of Adr on cell viability and invasion, while miR­130a knockdown enhanced the sensitivity of AML cells to Adr. Furthermore, Adr exerted an inhibitory effect on EMT in AML cells, which was rescued by miR­130a overexpression and enhanced by miR­130a knockdown. miR­130a knockdown also increased the sensitivity of AML cells to Adr by decreasing cell viability, invasion and EMT. Therefore, miR­130a knockdown is a potential therapeutic strategy for Adr­resistant AML.