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Oncology reports

miRNA-301a induces apoptosis of chronic myelogenous leukemia cells by directly targeting TIMP2/ERK1/2 and AKT pathways.


PMID 28035415

Abstract

We investigated the biological functions and mechanism of miRNA‑301a on apoptosis in chronic myelogenous leukemia (CML). The expression of miRNA‑301a in patient with CML cells was higher than the expression of normal patients. Overall survival (OS) of chronic granulocytic leukemia cell patient with low miRNA‑301 expression was superior to that of CML patient with high miRNA‑301 expression. Moreover, the upregulation of miRNA‑301a increased cell proliferation, inhibited apoptosis and caspase-3 and -9 activity of K562 cells. Next, the upregulation of miRNA‑301a suppressed Bax/Bcl-2 rate and TIMP2 protein expression, increased phosphorylation-ERK1/2 and decreased phosphorylation-AKT protein expression of K562 cells. Furthermore, si‑TIMP2 expression enhanced the upregulation of miRNA‑301a on the promotion of cell proliferation, inhibition of apoptosis and caspase-3 and -9 activity, suppression of Bax/Bcl-2 rate, increasing phosphorylation-ERK1/2 and decreasing phosphorylation-AKT protein expression of K562 cells. Taken together, our results clearly suggested that miRNA‑301a induces apoptosis of CML cells by directly targeting the TIMP2/ERK1/2 and AKT pathways.