Chen Qi, Guo Sheng Min, Huang Hou Qiang, Huang Guo Ping, Li Yi, Li Zi Hui, Huang Run, Xiao Lu, Fan Chun Rong, Yuan Qing, Zheng Si Lin
Nursing Department, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Rehabilitation Department, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Aging (Albany NY). 2020 Sep 25;12(18):17902-17920. doi: 10.18632/aging.103332.
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 . 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.
非小细胞肺癌（NSCLC）是一种难治性恶性肺癌，转移率和死亡率都很高。目前，长链非编码RNA（lncRNA）SBF2反义RNA 1（SBF2-AS1）被认为是多种肿瘤的生物标志物。然而，SBF2-AS1在NSCLC生长和转移中的作用仍需进一步研究。在本研究中，我们发现与正常组织相比，SBF2-AS1在NSCLC组织中过表达。沉默SBF2-AS1可抑制NSCLC细胞的生长和侵袭性表型。同样，敲低SBF2-AS1可阻碍NSCLC细胞在裸鼠体内的生长。接下来的荧光素酶报告基因检测和RNA免疫沉淀（RIP）检测表明了miR-338-3p与SBF2-AS1之间的关系。挽救实验表明，miR-338-3p抑制剂消除了SBF2-AS1沉默对NSCLC细胞生长、迁移和侵袭的抑制作用。荧光素酶报告基因检测和免疫印迹检测证实，解整合素金属蛋白酶17（ADAM17）是miR-338-3p的靶标。此外，SBF2-AS1通过吸附miR-338-3p正向调节ADAM17的水平。最后，我们发现SBF2-AS1通过调节miR-338-3p/ADAM17轴促进NSCLC细胞的增殖和转移表型。
