miR-137 downregulates c-kit expression in acute myeloid leukemia

- miR-137 targets the 3′-UTR of c-kit.
- miR-137 suppresses the expression and activities of c-kit in AML cell.
- Expression of miR-137 inversely correlates with c-kit in large clinical samples and cell lines.
- miR-137 inhibits proliferation, promotes apoptosis, and induces differentiation of c-kit+ AML cells.

The oncogene c-kit plays a vital role in the pathogenesis of acute myeloid leukemia (AML). However, the mechanism of microRNAs targeting c-kit in AML has not been determined in detail. Moreover, the role miR-137 in tumor cell proliferation remains controversial. The aim of this work was to verify whether miR-137 targets c-kit and to research the biological effects of restoring miR-137 expression in leukemia cells. We found that miR-137 binds specifically to the 3′-UTR of c-kit and suppresses the expression and activities of c-kit. There is a negative correlation between miR-137 and c-kit expression in both patients and cell lines determined by screening large clinical samples. We found that miR-137 can inhibit proliferation, promote apoptosis, and induce differentiation of c-kit+ AML cells. We determined that miR-137 can participate in the leukemogenesis by regulating c-kit, which could be used as a therapeutic target for acute myeloid leukemia.