SNHG6 functions as a competing endogenous RNA to regulate E2F7 expression by sponging miR-26a-5p in lung adenocarcinoma.

Increasing evidence has highlighted the pivotal roles of deregulated long non-coding RNAs (lncRNAs) in tumourigenesis. However, the biological functions and mechanisms of lncRNAs in human lung adenocarcinoma (LUAD) remain elusive. Small nucleolar RNA host gene 6 (SNHG6), a novel lncRNA, is aberrantly expressed in various cancers. In this study, SNHG6 was upregulated in LUAD tissues, and its upregulation was positively associated with advanced TNM stage, large tumour size and poor overall survival (OS) in LUAD patients. Gain- and loss-of-function experiments confirmed that SNHG6 promoted cell cycle progression, cell proliferation, migration and invasion, and epithelial-mesenchymal transition (EMT) in vitro. Animal experiments demonstrated that SNHG6 knockdown remarkably inhibited xenograft formation in vivo. Moreover, mechanistic experiments identified that SNHG6 functions as a competing endogenous RNA (ceRNA) through competitively sponging miR-26a-5p to regulate E2F7 expression, cell motility and EMT in LUAD cells. In summary, our findings reveal that SNHG6 may act as an oncogenic lncRNA in LUAD carcinogenesis by regulating the miR-26a-5p/E2F7 axis.