Long noncoding RNA SBF2-AS1 contributes to the growth and metastatic phenotypes of NSCLC via regulating miR-338-3p/ADAM17 axis

Qi Chen(Affiliated Hospital of Southwest Medical University), Sheng Min Guo(Affiliated Hospital of Southwest Medical University), Hou Qiang Huang(Affiliated Hospital of Southwest Medical University), Guo Huang(Zigong First People's Hospital), Yi Li(Southwest Medical University), Zi Hui Li(Affiliated Hospital of Southwest Medical University), Run Huang(Southwest Medical University), Lu Xiao(Affiliated Hospital of Southwest Medical University), Chun Rong Fan(Affiliated Hospital of Southwest Medical University), Qing Yuan(Southwest Medical University), Shouwen Zheng(Affiliated Hospital of Southwest Medical University)
Aging
September 25, 2020
Cited by 16Open Access
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Abstract

. Consistently, SBF2-AS1 knockdown hindered the growth of NSCLC cell in nude mice. The following luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay suggested the relationship between miR-338-3p and SBF2-AS1. The rescue experiments showed that miR-338-3p inhibitor abolished SBF2-AS1 silencing caused inhibition on the growth, migration and invasiveness of NSCLC cell. The luciferase reporter assay and immunoblotting assay validated that A Disintegrin and Metalloprotease 17 (ADAM17) was a target of miR-338-3p. In addition, SBF2-AS1 positively regulated the level of ADAM17 through sponging for miR-338-3p. Finally, we revealed that SBF2-AS1 contributed to the proliferation and metastatic phenotypes of NSCLC cell via regulating miR-338-3p/ADAM17 axis.


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