Long non-coding RNA GNAS-AS1 promotes cell migration and invasion via regulating Wnt/β-catenin pathway in nasopharyngeal carcinoma.

Abstract

The diagnosis and prognosis of nasopharyngeal cancer (NPC) are still difficult. To investigate the effect of long-chain non-coding RNA GNAS-AS1 (lncRNA GNAS-AS1) on proliferation, migration, and invasion of NPC, we carried out this research to illustrate the underlying mechanism. Real-time quantitative PCR was used to detect the expression of GNAS-AS1 in nasopharyngeal carcinoma cells. The effect of transfection of si-GNAS-AS1 on the growth of nasopharyngeal carcinoma SUNE-1 cells was analyzed by CCK-8 assay and colony formation assay. The effect of GNAS-AS1 on the migration and invasion of SUNE-1 cells was detected by transwell assay and Matrigel assay. The expression of C-myc, CyclinD, and MMP2 was detected by Western blot. The expression of β-catenin was detected by real-time quantitative PCR and Western blot. GNAS-AS1 was upregulated in NPC. GNAS-AS1 promoted cell proliferation, cell migration, and cell invasion in vitro. GNAS-AS1 exerted its function by regulating Wnt/β-catenin pathway. GNAS-AS1 functioned as an oncogenic role via mediating β-catenin expression. LncRNA GNAS-AS1 played an important role in the proliferation, migration, and invasion of NPC cells, suggesting that GNAS-AS1 may be an important gene related to the formation and progression of nasopharyngeal carcinoma. The completion of this study provides new potential therapeutic targets for nasopharyngeal carcinoma.