Abstract
BackgroundLong noncoding RNAs (LncRNAs) play critical roles in multiple biological processes implicated in the development and progression of cancers. Terminal differentiation-induced lncRNA (TINCR) has been demonstrated to be associated with the carcinogenesis of several cancers. However, little is known about the function and mechanism of TINCR in lung cancer. MethodsqRT-PCR was performed to measure the expression of TINCR, miR-544a or FBXW7 mRNA in lung cancer tissues or cells. FBXW7 protein level was detected via western blot analysis. Cell Counting Kit-8 (CCK-8) and transwell invasion analysis were used to assess the proliferative and invasive ability of lung cancer cells. Bioinformatic softwares, luciferase reporter assay, and RNA immunoprecipitation (RIP) were employed to explore the relationship between TINCR, miR-544a and FBXW7. ResultsTINCR expression was downregulated while miR-544a expression was upregulated in lung cancer tissues and cells. TINCR overexpression suppressed proliferation and invasion in lung cancer cells. Moreover, TINCR was confirmed as a molecular sponge of miR-544a. We further validated that miR-544a facilitated proliferation and invasion, and miR-544a could reverse TINCR-mediated anti-proliferation and anti-invasion effect in lung cancer cells. TINCR acted as a competing endogenous RNA (ceRNA) to sequester miR-544a from its target gene FBXW7. Finally, FBXW7 suppressed proliferation and invasion, and FBXW7 knockdown abolished the inhibition of TINCR on proliferation and invasion in lung cancer cells. ConclusionTINCR suppressed proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer, indicating that it might be a potential target for the therapy of lung cancer.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.