Research Paper Volume 12, Issue 18 pp 17902—17920
Long noncoding RNA SBF2-AS1 contributes to the growth and metastatic phenotypes of NSCLC via regulating miR-338-3p/ADAM17 axis
- 1 Nursing Department, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China
- 2 Rehabilitation Department, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China
- 3 Laboratory Medicine, Zigong Maternal and Child Care Service Centre, Zigong 643000, Sichuan, China
- 4 School of Basic Medicine, Southwest Medical University, Luzhou 646000, Sichuan, China
Received: January 23, 2020 Accepted: March 31, 2020 Published: September 25, 2020
https://doi.org/10.18632/aging.103332How to Cite
Copyright: © 2020 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Non-small cell lung cancer (NSCLC) is a type of refractory malignant lung cancer with a high rate of metastasis and mortality. Currently, long non-coding RNA (lncRNA) SBF2 Antisense RNA 1 (SBF2-AS1) is considered as a biomarker for a variety of tumors. However, the function of SBF2-AS1 in the growth and metastasis of NSCLC needs to be further studied. In this study, we revealed that SBF2-AS1 was overexpressed in NSCLC tissues compared with that in normal tissues. SBF2-AS1 silencing restrained the growth and aggressive phenotypes of NSCLC cell in vitro. 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.