LAUSR

Oral squamous cell carcinoma (OSCC) has increasingly become a worldwide health concern, and its survival rate has not been much improved partially due to a deficiency of precise molecular markers. Dysregulation of LINC01116, a long noncoding RNA sequence, has been observed in several types of cancer. However, the role played by LINC01116 in OSCC has not yet been fully elaborated. This study explored how LINC01116 was involved in the regulation of OSCC progression by analyzing expressions of LINC01116 in OSCC patients. The findings demonstrated upregulation of LINC01116 in OSCC tissues as opposed to regular oral mucosa, and overexpression of LINC01116 was correlated with advanced tumor status. LINC01116 knockdown using shRNA markedly reduced the OSCC cell invasion and migration in vitro. Moreover, the expression of LINC01116 was negatively correlated with that of microRNA-9-5p (miR-9). Luciferase reporter and loss-of-function assays demonstrated that LINC01116 functioned as a competing endogenous RNA (ceRNA) that could effectively sponge miR-9, thus regulating the derepression of matrix metalloproteinase 1 (MMP1). Furthermore, we confirmed that LINC01116 knockdown did not affect the expression of MMP1 messenger RNA (mRNA). Collectively, it is demonstrated in this study that overexpression of LINC01116 can promote the OSCC progression. The LINC01116–miR-9-MMP1 axis provides a novel insight into the OSCC pathogenesis and offers potential therapeutic targets against OSCC.