MiR-222 regulates the progression of oral squamous cell carcinoma by targeting CDKN1B.

OBJECTIVE The purpose of this study was to establish a causal relationship between microRNA (miR-222) and oral squamous cell carcinoma (OSCC). METHODS The cell viability of each treatment group was measured by MTT. The effects of miR-222 on cell metastasis and apoptosis were measured by transwell and flow cytometry. The targeting relationship between miR-222 and CDKN1B was verified by dual-luciferase reporter gene assay and Western blot. Cell derived xenograft was further constructed to verify the effect of miR-222 on tumor growth by observing tumor weight and volume. The proliferation of tumor tissue was determined by hematoxylin-eosin staining and immunohistochemical staining. RESULTS Compared with those in adjacent tissues and normal cells, the levels of miR-222 in OSCC tissues and cells were significantly increased (P<0.05). The miR-222 mimic group promoted tumor cell proliferation, migration and cell cycle and inhibited cell apoptosis significantly (P<0.05). The up-regulation of CDKN1B expression inhibited cell viability, migration and invasiveness and promoted the apoptosis of OSCC (P<0.05). The dual-luciferase reporter gene assay found that miR-222 was targeted to CDKN1B and could inhibit fluorescence activity (P<0.05). In vivo assays showed that miR-222 could promote tumor growth through CDKN1B (P<0.05). CONCLUSION MiR-222 was significantly upregulated in OSCC tissues and cells and regulated tumor progression by targeting CDKN1B.