Emerging evidence has indicated that microRNAs are involved in tumor development and progression, acting as either tumor suppressors or oncogenes. In this study, we aimed to investigate the role of miR-130a in the pathogenesis of chronic myeloid leukemia (CML). Functional studies indicate that over-expression of miR-130a in A562 CML cells dramatically suppresses cell proliferation and induces cell apoptosis both in vitro and in vivo. Furthermore, we demonstrate that the transcriptional regulator RECK is a target of miR-130a. In conclusion, our study suggests that miR-130a may function as a novel tumor suppressor in CML, and its anti-oncogenic activity may involve the direct targeting and inhibition of RECK.
Keywords: A562; Chronic myeloid leukemia (CML); RECK; invasion; miR-130a; migration; target therapy.