LINC01518 functions as an oncogene in head and neck squamous cell carcinoma (HNSCC) by modulating miR-1-3p/Slug and miR-216b-5p/GRP78 axis

Abstract

Abstract HNSCC is a highly aggressive cancer of the head and neck region, and there is an urgent need to find novel potential targets for its diagnosis and treatment. Long non-coding RNAs (lncRNAs) have emerged as important therapeutic and diagnostic targets for multiple cancers, including HNSCC. LINC01518 promotes the proliferation of oesophageal cancer cells, but the involvement of LINC01518 in HNSCC pathophysiology is unknown. We show that LINC01518 expression is significantly upregulated in high-grade HNSCC tumor samples in comparison to normal tissue, and transforming growth factor- β (TGF-β) promotes LINC01518 expression in HNSCC cell lines. Loss-of-function studies suggest that LINC01518 promotes cell proliferation, migration, and invasion in HNSCC cells. In addition, LINC01518 depletion sensitizes HNSCC cells to cisplatin-mediated apoptosis. Mechanistically, LINC01518 acts as a competitive endogenous RNA and binds to miR-1-3p and miR-216b-5p, resulting in up-regulation of their target genes Slug and GRP78, respectively. Our findings suggest that LINC01518 is an attractive therapeutic target for HNSCC.