LAUSR

Objective We attempted to clarify the effect of lncRNA MSC-AS1 on carcinogenic and development of nasopharyngeal carcinoma (NPC) and the related mechanisms. Methods The levels of MSC-AS1 and miR-429 were estimated in NPC tissues and cells using qRT-PCR. Correlation analysis, dual-luciferase report, and RNA pull down assay assessed the action association of MSC-AS1 and miR-429. MTT, colony formation, cell wound scratch, and transwell assays were used to assess the proliferation, invasion, and migration of C666-1 cells. Metastasis-related protein expressions and activation of the JAK1/STAT3 pathway were confirmed by western blot and immunohistochemistry. Results The expression of MSC-AS1 presented significant upregulation, and miR-429 expression was markedly downregulated in NPC tissues and cells. The level of MSC-AS1 had negative relation to the miR-429 level. Knockdown of MSC-AS1 suppressed the proliferation, invasion, and migration of C666-1 cells. On the contrary, overexpressing of MSC-AS1 exerts the opposite effects on C666-1 cell growth and migration. miR-429 was determined as functional downstream of MSC-AS1. The suppressive function of MSC-AS1 knockdown was predominately abolished by the miR-429 inhibitor. miR-429 was an antitumor gene inhibiting NPC growth and metastasis through JAK1/STAT3 pathway. In C666-1 cells, the elevated cell growth and migration induced by the miR-429 inhibitor were significantly reversed by si-JAK1 transfection. Conclusions High expression of MSC-AS1 exerted a carcinogenic effect on NPC cell growth and metastasis by inhibiting miR-429 and activating the JAK1/STAT3 pathway.