MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin

This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT-qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-kappa B signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-kappa B signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.