LncRNA SNHG15 promotes the proliferation of nasopharyngeal carcinoma via sponging miR-141-3p to upregulate KLF9

OBJECTIVE: Long non-coding RNAs (IncRNAs) have been identified to exert an oncogenic or anti-tumor function in malignant tumors. LncRNA SNHG15 is verified to be an oncogene in hepatocellular carcinoma, colorectal cancer, and prostate cancer. In this paper, we mainly investigate the potential influence of SNHG15 on the progression of nasopharyngeal carcinoma (NPC). PATIENTS AND METHODS: SNHG15 levels in NPC tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between SNHG15 level and prognosis of NPC patients was evaluated by the Kaplan-Meier method. Regulatory effects of SNHG15 on proliferative, colony formation abilities, and apoptosis of SUNE1 and CNE1 cells were assessed through a series of functional experiments. Potential miRNAs binding SNHG15 and the downstream gene of the microRNA (miRNA) were predicted by bioinformatics method, which was confirmed by Dual-Luciferase reporter gene assay and Western blot. RESULTS: SNHG15 was upregulated in NPC tissues and cells. High level of SNHG15 indicated worse survival in NPC patients. Knockdown of SNHG15 markedly suppressed proliferative ability and induced apoptosis in SUNE1 and CNE1 cells. It is verified that miR-141-3p was the direct target binding SNHG15, and KLF9 was the downstream gene of miR-141-3p. SNHG15 was demonstrated to be a ceRNA to upregulate KLF9 by competitively binding miR-141-3p. CONCLUSIONS: SNHG15 is upregulated in NPC tissues, and this aggravates the progression of NPC by absorbing miR-141-3p to upregulate KLF9.