Downregulation of LINC00460 decreases STC2 and promotes autophagy of head and neck squamous cell carcinoma by up-regulating microRNA-206.

Aim: Head and neck squamous cell carcinoma (HNSCC) is one of the most prevalent types of cancer worldwide with unfavorable patient outcomes and relatively low survival rates. Long non-coding RNAs (lncRNAs) have been demonstrated to participate in the progression of HNSCC. The present study aimed to investigate the functional mechanism of lncRNA LINC00460 in HNSCC by mediating microRNA-206 (miR-206)/stanniocalcin-2 (STC2) axis.

Methods: The interactions among miR-206, LINC00460 and STC2 were identified, and the expression of LINC00460, miR-206 and STC2 in tissues and cells was determined. Gain- and loss-of function experiments were conducted to analyze effects of LINC00460, miR-206 and STC2 on the expression of apoptosis-related proteins, autophagy-related proteins, and the extents of AKT, ERK phosphorylation. Cell cycle distribution, apoptosis and the production of autophagosomes after transfection were evaluated to further explore the role of LINC00460/miR-206/STC2 axis in HNSCC.

Results: LINC00460 and STC2 were highly expressed while miR-206 was poorly expressed in HNSCC. Besides, miR-206 was found to bind to both LINC00460 and STC2. After the transfection of HNSCC cells with miR-206 mimic or si-LINC00460, the expression of STC2, AKT, ERK, as well as the extent of AKT, ERK phosphorylation all decreased, which facilitated the apoptosis and autophagy of HNSCC cells.

Conclusion: Collectively, the apoptosis and autophagy of HNSCC can be facilitated by downregulating LINC00460, which highlights a novel target in the treatment of HNSCC.