miR-125a regulates cell cycle, proliferation, and apoptosis by targeting the ErbB pathway in acute myeloid leukemia

MicroRNA profiling of acute myeloid leukemia (AML) patient samples revealed a decrease in miR-125a expression. While the role of miR-125a in normal hematopoiesis has been studied, its involvement in AML remains unexplored. Analysis of the upstream region of miR-125a identified several CpG islands. Treatment with the de-methylating agent Decitabine led to an increase in both precursor and mature forms of miR-125a. Profiling further revealed a significant reduction in the ErbB signaling pathway following ectopic expression of miR-125a. Both ectopic miR-125a expression and ErbB inhibition via Mubritinib suppressed cell cycle proliferation and progression, while promoting apoptosis. These findings suggest that ErbB inhibitors may represent a promising novel therapeutic strategy for treating AML characterized by low miR-125a levels.