Increasing evidence has been suggested that microRNA-144 (miR-144) involved in tumor initiation, development and metastasis in various cancers. However, the biological roles and potential mechanisms of miR-144 in laryngeal squamous cell carcinoma (LSCC) remain unclear. In the present study, we discovered that miR-144 expression levels in LSCC tissues were significantly lower than those of adjacent normal tissues. Furthermore, overexpression of miR-144 in LSCC cells inhibited cell proliferation, colony formation, migration, and invasion in vitro. Consistently, stable overexpression of miR-144 suppressed the growth of LSCC cell xenografts in vivo. Bioinformatic algorithms and luciferase reporter assays confirmed that insulin receptor substrate 1 (IRS1) is a direct target of miR-144. Overexpreesion of miR-144 obviously decreased IRS1 expression thereby suppressing phosphatidylinositol 3-kinase (PI3K)/AKT pathway activation. Further functional studies suggested that downregulation of IRS1 had similar effects as that of miR-144 overexpression, and upregulation of IRS1 partially reversed the inhibitory effects of miR-144. These findings suggested that miR-144 functioned as a tumor suppressor in LSCC by targeting IRS1, and that miR-144 might serve as a potential target for LSCC treatment.
Keywords: IRS1; growth; laryngeal squamous cell carcinoma; metastasis; miR-144.