Function of miR‑152 as tumor suppressor in oral squamous cell carcinoma cells by targeting c‑MET

MicroRNA‑152 (miR‑152) has been reported to be involved in tumor development and progression in multiple cancers. However, the expression level, biological function and regulatory mechanisms of miR‑152 in oral squamous cell carcinoma cells (OSCC) remain unclear. The aims of this study were therefore to investigate the role of miR‑152 in OSCC and the relevant mechanism. It was found that miR‑152 was downregulated in OSCC cell lines and tissues, and that decreased miR‑152 was closely associated with lymph node metastasis, and patient survival rate. In vitro restoration of miR‑152 significantly repressed cell proliferation, colony formation, migration and invasion of OSCC cells. Notably, cellular-mesenchymal to epithelial transition factor (c‑MET) and its downstream signaling pathway (PI3K/Akt) was downregulated in OSCC cells by miR‑152 through direct interactions with its 3' untranslated region. Restoring c‑MET expression attenuated miR‑152-induced inhibitory effects in OSCC cells. In vivo study confirmed that restoration of miR‑152 suppressed tumor growth in xenograft nude mice by repressing c‑MET. In summary, the present study highlight miR‑152 as a tumor suppressor in OSCC through direct targeting c‑MET, rendering miR‑152 a promising therapeutic target for oral squamous cell carcinoma.