LAUSR

Laryngeal cancer (LC) is an increasingly common malignant tumors of head and neck cancer. Aberrant expression of microRNA (miRNA) is closely related with LC development. In the current study, we investigated the biological function and underlying molecular mechanism of miR‐384 in LC. The results showed that the miR‐384 expression was markedly downregulated in LC tissue and cell lines (TU212 and TU686) as compared with that of adjacent nontumor tissues and a normal human bronchial epithelial cell line. Next, we performed gain‐of‐function and loss‐of‐function experiments in the TU212 and TU686 cells by transfecting the cells with miR‐384 mimics, miR‐384 inhibitor, or miRNA control. Moreover, results showed that miR‐384 mimic remarkably inhibited LC cell proliferation, which was notably decreased by miR‐384 inhibitor. Furthermore, miR‐384 mimics notably increased the amounts of DNA fragmentation from the apoptotic cells (a hallmark of apoptosis) and the caspase‐3 activity, whereas miR‐384 inhibitor resulted in a decline of DNA fragmentation and the caspase‐3 activity compared with its control. In addition, a dual‐luciferase reporter assay confirmed that Wnt‐induced secreted protein‐1 (WISP1) gene was a direct target of miR‐384. MiR‐384 mimic remarkably inhibited the messenger RNA and protein expression of WISP1, which was upregulated by miR‐384 inhibitor as compared to its control. WISP1 knockdown by small interfering RNA inhibited LC cell proliferation and promoted cell apoptosis. WISP1 overexpression partly abrogates the effect of miR‐384 overexpression. Taken together, these data indicate that miR‐384 regulates LC cell proliferation and apoptosis through targeting WISP1 signaling pathway, providing a novel insight into the LC treatment.