Knockdown of SNHG12 suppresses tumor metastasis and epithelial-mesenchymal transition via the Slug/ZEB2 signaling pathway by targeting miR-218 in NSCLC.

Non-small cell lung cancer (NSCLC) is a type of lung cancer which has a high mortality and low survival rate. Previous studies have revealed that long non-coding RNAs participate in tumorigenesis and metastasis in NSCLC. In the present study, the function of small nucleolar RNA host gene 12 (SNHG12) was investigated in NSCLC. Using reverse transcription-quantitative polymerase chain reaction analysis, it was identified that SNHG12 was significantly overexpressed in NSCLC specimens. Furthermore, overexpression of SNHG12 was identified to be associated with tumor progression and poor overall survival rates. Knockdown of SNHG12 in NSCLC cells could effectively induce cell apoptosis and suppress cell viability, proliferation, migration and invasion via inhibition of the epithelial-mesenchymal transition process. Furthermore, a direct interaction between microRNA (miR)-218 and the binding site of SNHG12 was identified. SNHG12 acted as an endogenous sponge for miR-218. Knockdown of SNHG12 upregulated the expression level of miR-218 as well as downregulating the Slug/zinc finger E-box-binding homeobox 2 EMT signaling pathway, and thus inhibited cell migration and invasion. Therefore, SNHG12 may serve as a key biomarker and a potential therapeutic target for the treatment of NSCLC.