Suppressed Proliferation and Promoted Apoptosis in Laryngeal Squamous Cell Carcinoma by Targeting and Modifying ULK2.

PURPOSE

Long noncoding RNAs growth arrest-specific 5 () exerts important functions in modulating various tumor behaviors. However, the role of lncRNA in laryngeal squamous cell carcinoma (LSCC) remains unknown.

MATERIALS AND METHODS

Cell viability and apoptosis were, respectively, detected by cell counting kit-8 and flow cytometry, DIANA-LncBase V, Starbase, TargetScan and a dual-luciferase reporter gene assay were employed to assess the relationship among , miR-26a-5p and uncoordinated 51-like kinase 1 (ULK2), and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were performed to detect the expression of autophagy-relative factors.

RESULTS

The expression level of was frequently decreased in LSCC cell lines, and up-regulated inhibited AMC-HN-8 cells viability and induced apoptosis. More importantly, we found that activated autophagy, with enhanced autophagy-related proteins after overexpression. While down-regulated had opposite results in Tu 177 cells, was found to act as a microRNA sponge in a pathway to regulate miR-26a-5p and its target gene ULK2. MiR-26a-5p mimics inhibited apoptosis and autophagy, which were reversed by and si in AMC-HN-8 cells and Tu 177 cells, as well as ULK2 in AMC-HN-8 cells. Meanwhile, the concomitant downregulation of ULK2 and miRNA-26a-5p inhibitor decreased the miRNA-26a-5p inhibitor-induced apoptosis and autophagy.

CONCLUSION

This is the first report of LncRNA acting as a tumor suppressor in LSCC by regulating the miR-26a-5p/ULK2 axis, and it could be a new target for gene therapy in LSCC.