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C-kit is an oncogene that encodes a tyrosine kinase receptor called C-KIT (CD117). C-KIT is expressed in over 68% of Acute Myeloid Leukemia (AML) cells and it has been reported to play a crucial role in the pathogenesis of AML.1 Additionally, AML patients with C-KIT mutations often display drug resistance and inefficiency to clinical treatment. MicroRNAs (miRNA) have been reported to regulate C-KIT function. miR-137 has been shown to play a role in the pathogenesis of tumors, however, its precise role specifically in AML has not been elucidated yet.2
In an article published in Leukemia Research, Yanping Hu and colleagues from the Shengjing Hospital of China Medical University, PR China, discuss their findings from their study, which investigated the mechanism by which miR-137 regulates c-kit in AML samples.
In summary, the results of this study show that a decrease in miR-137 level correlates with an increase in c-kit expression level in AML. Additionally, miR-137 targets the 3’UTR of c-kit and this leads to the downregulation of C-KIT protein levels. Furthermore, miR-137 can inhibit proliferation, and increase apoptosis and differentiation of AML cells, thus indicating that miR-137 downregulation of C-KIT plays a role in the pathogenesis of AML.
In conclusion, dysregulation of miR-137 can participate in the development of c-kit+ AML. The authors suggested that regulation of miR-137 expression can be an effective therapeutic strategy for patients with c-kit driven AML.
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.
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