Abstract
Oral cancer is one of the common cancers worldwide, among which over 90% are oral squamous cell carcinomas (OSCC). MicroRNAs act as critical regulators of cancer development and progression. MiR-103a-3p has been reported to be upregulated in OSCC patients and closely correlated to poor prognosis, yet its roles in the progression of OSCC remain undisclosed. In this study, we knocked down the expression of miR-103a-3p in two OSCC cell lines in vitro, and significantly repressed cell proliferation and cell cycle arrest at the G1 phase were observed, accompanied by decreased proliferating cell nuclear antigen, cyclin D1, cyclin B1 and increased PTEN levels. MiR-103a-3p inhibition also induced apoptosis as evidenced by increased apoptotic cells and upregulated cleaved caspase-9/casapase-3 expression. We established a xenograft model in nude mice and found that miR-103a-3p knockdown also suppressed tumor growth in vivo. Besides, the expression of regulator of calcineurin1 (RCAN1), known as its anti-tumor effect, was negatively correlated with the miR-103a-3p level in OSCC cells. We validated that RCAN1 was a downstream target of miR-103a-3p using the dual-luciferase assay. RCAN1 silencing reversed the cell proliferative inhibition, cell cycle arrest and cell apoptosis induced by miR-103a-3p knockdown. In addition, we found that long non-coding RNA LINC00675 acted as a sponge of miR-103a-3p and promoted the expression of miR-103a-3p targets RCAN1 and PTEN. In summary, miR-103a-3p inhibition represses proliferation and induces apoptosis of OSCC cells through regulating RCAN1, and miR-103a-3p may act as a novel diagnostic marker and therapeutic target for OSCC.