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Long noncoding antisense RNA FAM83A‐AS1 promotes lung cancer cell progression by increasing FAM83A
Author(s) -
Shi Rongxing,
Jiao Zichen,
Yu Ao,
Wang Tao
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28336
Subject(s) - antisense rna , long non coding rna , rna , dna , gene , downregulation and upregulation , biology , cell , lung cancer , cancer , cell culture , cancer research , microbiology and biotechnology , genetics , medicine
The abnormal expression of long noncoding RNAs (lncRNAs) is closely associated with human cancers. As one special group of lncRNAs, natural antisense transcripts (NATs) can be transcribed from both DNA strands at the same locus but in the opposite direction from the gene transcript. Their expression levels are altered in many cancers, but their roles are poorly understood. We strove to find NATs involved in human non–small‐cell lung cancer (NSCLC) and to reveal their mechanism of action in cancer. We analysed the NATs in NSCLC from the TCGA database by circlncRNAnet. One NAT, family with sequence similarity 83 member A antisense RNA 1 (FAM83A‐AS1), was found to be markedly upregulated and positively correlated with its cognate sense counterpart, FAM83A, in NSCLC. Moreover, overexpression of FAM83A‐AS1 increased FAM38A protein levels and induced ERK1/2 phosphorylation downstream of FAM83A in cells. Finally, overexpression of FAM83A‐AS1 promoted LUAD cell proliferation and invasion. In summary, lncRNA FAM83A‐AS1 promotes LUAD by increasing FAM83A expression.