MicroRNA-19a functions as an oncogenic microRNA in non-small cell lung cancer by targeting the suppressor of cytokine signaling 1 and mediating STAT3 activation.

Abstract MicroRNA‑19a (miR‑19a) has been found to be overexpressed in lung cancers. However, the underlying molecular mechanisms of miR‑19a in tumorigenesis and the development of lung cancer remain poorly understood. In the present study, we aimed to delineate the role and mechanisms of action of miR‑19a in non‑small cell lung cancer (NSCLC). miR‑19a was found to be overexpressed in both NSCLC tumor tissues and cell lines, as shown by RT-PCR. The enforced expression of miR‑19a by transfection with miR-19a mimics significantly enhanced cell growth and viability, cell invasion and the migration of NSCLC cells, as shown by cell invasion and migration assays, and promoted the growth of xenograft tumors in a mouse xenograft tumor model. Conversely, the inhibition of miR‑19a by transfection of the cells with miR‑19a inhibitor displayed the opposite effects. More importantly, we found that miR‑19a directly interacted with the 3'‑untranslated region (3'‑UTR) of the suppressor of cytokine signaling 1 (SOCS1) by dual‑luciferase reporter assay. miR‑19a was found to be capable of regulating the expression of SOCS1 in NSCLC cells. Thus, by modulating SOCS1 expression, miR‑19a regulated the expression of the signal transducer and activator of transcription 3 (STAT3). Taken together, our data provide a possible underlying mechanism of action of miR‑19a in the development of NSCLC and suggest that miR‑19a may be a novel and promising target for therapeutic intervention in NSCLC.