长链非编码反义RNA FAM83A-AS1通过增加FAM83A促进肺癌细胞进展。
Long noncoding antisense RNA FAM83A-AS1 promotes lung cancer cell progression by increasing FAM83A.
作者信息
Shi Rongxing, Jiao Zichen, Yu Ao, Wang Tao
机构信息
Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.
Department of Cardiothoracic Surgery, Nanjing Drum Tower Hospital, Nanjing Medical University, Nanjing, China.
出版信息
J Cell Biochem. 2019 Jun;120(6):10505-10512. doi: 10.1002/jcb.28336. Epub 2019 Jan 18.
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.
长链非编码RNA(lncRNAs)的异常表达与人类癌症密切相关。作为lncRNAs的一个特殊群体,天然反义转录本(NATs)可以从同一位点的两条DNA链上转录,但方向与基因转录本相反。它们的表达水平在许多癌症中发生改变,但其作用却知之甚少。我们致力于寻找参与人类非小细胞肺癌(NSCLC)的NATs,并揭示它们在癌症中的作用机制。我们通过circlncRNAnet分析了来自TCGA数据库的NSCLC中的NATs。发现一种NAT,序列相似性家族83成员A反义RNA 1(FAM83A-AS1),在NSCLC中显著上调,并且与其同源的正义对应物FAM83A呈正相关。此外,FAM83A-AS1的过表达增加了FAM38A蛋白水平,并在细胞中诱导了FAM83A下游的ERK1/2磷酸化。最后,FAM83A-AS1的过表达促进了LUAD细胞的增殖和侵袭。总之,lncRNA FAM83A-AS1通过增加FAM83A的表达促进LUAD。