Abstract
Abstract In this study, we report that long non-coding RNA (lncRNA) SNHG16 is upregulated in non-small cell lung cancer (NSCLC) tissues, and is correlated with tumor size, TNM stage and lymph node metastasis. Kaplan-Meier analysis shows that the patients with high SNHG16 expression have poorer disease-free survival (DFS) and overall survival (OS) than the patients with low SNHG16 expression. Multivariate Cox regression analysis reveals that SNHG16 expression could be regarded as an independent predictor for DFS and OS in NSCLC patients. In vitro experiments show that SNHG16 knockdown inhibits NSCLC cell proliferation, migration and invasion, and SNHG16 overexpression promotes NSCLC cell proliferation, migration and invasion. We further identify and confirm that miR-146a is the target of SNHG16, and SNHG16 functions by targeting miR-146a. Subsequently, MUC5AC, a major mucin in the human respiratory tract correlated with post-operative metastasis and recurrence of NSCLC, is confirmed to be regulated by SNHG16 and miR-146a, and might be involved in the oncogenic activity of SNHG16-miR-146a axis in NSCLC. In vivo experiments also confirm these conclusions. Taken together, the present results elucidate a potential mechanism underlying the carcinogenesis role of SNHG16 in NSCLC, and indicate that SNHG16 could act as a novel promising marker for prognosis, and a potential therapeutic target for NSCLC treatment in the future.
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