Abstract
Long non-coding RNAs (lncRNAs) have been proposed to correlate with various carcinomas, yet the role of lncRNA SNHG7 in nasopharyngeal carcinoma (NPC) is hardly studied. This study intends to examine the molecular mechanism of SNHG7 on NPC cells. The NPC tissues and nasopharyngeal tissues of mild inflammation of nasopharyngeal mucosa were obtained. SNHG7, miR-140-5p, and GLI3 mRNA and protein expression in tissues and in the CNE1, HONE1, C666-1, CNE2, and normal NP69 cell lines was detected. IC50 and the protein expression of related drug-resistant genes of CNE2 and CNE2/DDP cells were determined. Proliferative ability, cell colony formation rate, cell cycle, and apoptosis of CNE2 and CNE2/DDP cells were also detected. SNHG7, miR-140-5p, and GLI3 mRNA and protein expression in CNE2 and CNE2/DDP cells in each group was detected. SNHG7's cell localization, the binding sites of SNHG7 and miR-140-5p along with miR-140-5p and GLI3 were detected. Overexpressed SNHG7 and GLI3, and underexpressed miR-140-5p were found in NPC tissues and cells. SNHG7 silencing and miR-140-5p elevation declined the drug resistance of drug-resistant NPC cells and their parent cells, restrained NPC cell colony formation ability and proliferation, and boosted cell apoptosis. SNHG7 specially bound to miR-140-5p, and SNHG7 silencing elevated miR-140-5p expression. GLI3 was a direct target gene of miR-140-5p and miR-140-5p elevation diminished GLI3 expression. MiR-140-5p inhibition reversed the impacts of SNHG7 silencing on NPC cells. In summary, our study reveals that downregulated SNHG7 restricts GLI3 expression by upregulating miR-140-5p, which further suppresses cell proliferation, and promotes apoptosis of NPC.