<scp>LncRNA FAM83A‐AS1</scp> promotes <scp>lung adenocarcinoma</scp> progression by enhancing the <scp>pre‐mRNA</scp> stability of <scp>FAM83A</scp>
Wenyi Wang, Zhunlin Zhao, C. F. Xu, Chang Li, Cheng Ding, Jun Chen, Tengfei Chen, Jun Zhao
Abstract
BACKGROUND: Lung cancer is the leading cause of cancer deaths worldwide. Long non-coding RNAs (lncRNAs) affect a series of cellular biological processes, including oncogene function promotion. In this study, we explored the functions and mechanisms of FAM83A antisense RNA 1 (FAM83A-AS1) in non-small cell lung cancer (NSCLC) progression. METHODS: The expression of FAM83A-AS1and FAM83A mRNA was analyzed using the Cancer Genome Atlas (TCGA) data. Proliferation, migration, invasion and Western blotting were measured after treatment with overexpressed or knockdown FAM83A-AS1. To determine the relationship between FAM83A-AS1 and FAM83A, RNase protection assay (RPA), amanitin treatment, RNA pulldown assay and RNA immunoprecipitation (RIP) assay were performed. RESULTS: High expression of FAM83A-AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression-free survival (PFS). Functionally, high FAM83A-AS1 expression increased LUAD cell proliferation and metastasis, indicating that FAM83A-AS1 exerted its oncogenic functions. Furthermore, FAM83A-AS1 promoted NSCLC progression via ERK signaling pathways. Mechanistically, FAM83A-AS1 post-transcriptionally increased FAM83A expression by enhancing pre-mRNA stability. FAM83A-AS1 enhanced FAM83A mRNA stability not only by forming an RNA duplex but also by binding to FBL. CONCLUSIONS: We determined that FAM83A-AS1 increased FAM83A expression by enhancing FAM83A pre-mRNA stability and promoted the tumorigenesis of LUAD.