Abstract
This work expanded the knowledge of the molecular mechanisms underlying LC progression by exploring the role of miR-892a in the viability of TU212 and M4E cells. The results showed that miR-892a, which exhibited elevated expression in LC cells and tissue specimens of patients with LC, exerted an inhibitory effect on Dicer expression, whereas silencing of miR-892a in TU212 and M4E cells hindered cell proliferation and growth and promoted apoptosis. Furthermore, miR-892a was demonstrated to directly target Dicer 3'-UTR and inhibit its expression. These findings demonstrated that miR-892a acted as an LC oncogene via its action on Dicer, which further confirmed that miR-892a can serve as a diagnostic indicator or promising agent for LC treatment.
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