SNHG20 knockdown suppresses proliferation, migration and invasion, and promotes apoptosis in non-small cell lung cancer through acting as a miR-154 sponge

• Main Authors: Jin Lingling, Jiang Xiangao, He Guiqing, Shi Jichan, Su Feifei, Zhu Haiyan
• Format: Article
• Language: English
• Published: Elsevier 2019-04-01
• Series: Biomedicine & Pharmacotherapy
• Subjects: lncRNA SNHG20; Competing endogenous RNA; NSCLC; Proliferation; Migration; Invasion
• Online Access: http://www.sciencedirect.com/science/article/pii/S0753332218383756

Long noncoding RNAs (LncRNAs) play critical roles in the development and progression of cancers. However, little is known about the function and mechanism of lncRNAs in non-small cell lung cancer (NSCLC). In this study, we investigated the expression and functional role of lncRNA small nucleolar RNA host gene 20 (SNHG20) as well as its underlying mechanism in NSCLC. Our results showed that SNHG20 was significantly up-regulated in NSCLC tissues and cells. High SNHG20 expression was implicated with poor prognosis in NSCLC patients. Moreover, SNHG20 knockdown suppressed proliferation, migration and invasion, and induced apoptosis in NSCLC cells. Furthermore, SNHG20 could function as a competing endogenous RNA (ceRNA) to elevate ZEB2 and RUNX2 expression by sponging miR-154. Rescue assays revealed that miR-154 inhibition could reverse the inhibitory effect of SNHG20 silence on proliferation, migration and invasion in NSCLC cells. More importantly, SNHG20 knockdown suppressed tumor growth in NSCLC in vivo through suppressing miR-154 and elevating ZEB2 and RUNX2 expression. In summary, knockdown of lncRNA SNHG20 suppressed proliferation, migration and invasion, and promotes apoptosis through up-regulating ZEB2 and RUNX2 expression by sponging miR-154 in NSCLC, providing a promising therapeutic target for NSCLC patients.