Abstract
LncRNAs (long noncoding RNAs) have been shown to be potentially critical regulators in head and neck squamous cell carcinoma (HNSCC). LncRNA LINC00460 (long intergenic non-protein coding RNA 460), an "oncogene", regulates progression of various tumors. However, the tumorigenic mechanism of LINC00460 on HNSCC is yet to be investigated. In the current study, we discovered that LINC00460 was relatively up-regulated in both HNSCC cancer tissues and cell lines, and predicted a poor prognosis in HNSCC patients. Gain- and loss-of functional studies established that over-expression of LINC00460 promoted cell proliferation, invasion and migration of HNSCC cells in vitro, while the promotion abilities were suppressed via knockdown of LINC00460. Our results identified miR-612 as a novel target of LINC00460, whose expression suggested a negative correlation with LINC00460 in HNSCC tissues and cell lines. LINC00460 increased the expression of serine/threonine kinase AKT2 via sponging miR-612. Rescue experiments indicated that LINC00460 could promote HNSCC progression partially through inhibition of miR-612. Subcutaneous xenotransplanted tumor model confirmed that interference of LINC00460 suppressed in vivo tumorigenic ability of HNSCC via down-regulation of AKT2. In conclusion, our findings clarified the biologic significance of LINC00460/miR-612/AKT2 axis in HNSCC progression and provided novel evidence that LINC00460 may be a new potential therapeutic target for HNSCC.