Knockdown SNHG20 Suppresses Nonsmall Cell Lung Cancer Development by Repressing Proliferation, Migration and Invasion, and Inducing Apoptosis by Regulating miR-2467-3p/E2F3

Lung cancer was one of the most common malignant tumors worldwide. In China, lung cancer has become the leading reason of malignant tumors-related mortality in urban population, whereas nonsmall cell lung cancer (NSCLC) represented at least 80% of all lung cancers with poor 5-year survival rate. Long noncoding RNA (lncRNA) small nucleolar RNA host gene 20 (SNHG20) was reported to be associated with NSCLC, but the regulatory mechanisms of SNHG20 in NSCLC needed further investigation.

SNHG20 contributed to NSCLC development through mediating AKT signaling pathway and sponging miR-2467-3p to elevate E2F3 expression in NSCLC cells.

The abundances of SNHG20 and E2F transcription factor 3 (E2F3) in NSCLC tissues and cells were measured with real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assays. 3-(4, 5-Dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) was applied to detect cells proliferation, whereas flow cytometry analysis was used to monitor cell apoptosis. In addition, cells capabilities of migratory and invasion were assessed with transwell assay. The association among miR-2467-3p, SNHG20, and E2F3 was analyzed by dual-luciferase reporter assay. The related protein expression levels were determined by Western blot.

SNHG20 and E2F3 was upregulation in NSCLC tissues and cell lines. Mechanical experiment displayed that knockdown of SNHG20 or E2F3 silencing could inhibit proliferation, motility, and improve apoptosis in NSCLC cell lines. Restored expression of E2F3 could effectively reverse reduction of proliferation, motility, and promotion of apoptosis caused by SNHG20 silencing in NSCLC cells. Besides, SNHG20 activated protein kinase B (AKT) signaling pathway and increased E2F3 level in NSCLC cells through targeting miR-2467-3p.