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.
Conclusions
We determined that FAM83A-AS1 increased FAM83A expression by enhancing FAM83A pre-mRNA stability and promoted the tumorigenesis of LUAD.
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.