Abstract
LINC01234 plays a pivot role in the tumorigenesis of gastric cancer, colon cancer and lung cancer. However, how LINC01234 participates in oral squamous cell carcinoma (OSCC) progression remains unknown. In our research, we showed that LINC01234 was dramatically upregulated in OSCC tissues. And interestingly, high LINC01234 expression predicted a low overall survival rate in OSCC patients. Knockdown of OSCC inhibited the proliferation of cancer cells and led to more cells restricted in G0 phase. Moreover, LINC01234 silencing decreased the migration and invasion of OSCC cells. Additionally, downregulation of LINC01234 limited OSCC tumor propagation in vivo. Mechanistic investigation elucidated that LINC01234 inhibited the activity of miR-637 to increase the expression of NUPR1. Via upregulating NUPR1 level, LINC01234 contributed to malignant behaviors of OSCC cells. Collectively, our research shows that LINC01234 exerts an important role in OSCC progression via miR-637/NUPR1 axis.
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