The long noncoding RNA colon cancer‐associated transcript‐1/miR‐490 axis regulates gastric cancer cell migration by targeting hnRNPA1. Issue 3 (30th January 2016)

• Record Type: Journal Article
• Authors: Zhou, Baoguo; Wang, Yuli; Jiang, Jinpeng; Jiang, Hongpeng; Song, Jianwei; Han, Taotao; Shi, Juan; Qiao, Haiquan
• Is Part Of: IUBMB life. Volume 68:Issue 3(2016)
• Page Start: 201
• Page End: 210
• Publication Date: 2016-01-30
• Subjects: lncRNA CCAT1/miR‐490 -- gastric cancer -- hnRNPA1; Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.1474
• Languages: English
• ISSNs: 1521-6543

Abstract

Abstract: Colon cancer‐associated transcript‐1 (CCAT1) is a highly conserved long noncoding RNA that is deregulated in several cancers. However, its role in gastric carcinoma and its post‐transcriptional regulation remain poorly understood. In this study, we provide the first evidence that CCAT1 regulates miR‐490 in gastric cancer (GC) cells. Interestingly, miR‐490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR‐490 expression was downregulated in GC. The negative correlation between miR‐490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR‐490‐binding site, and deletion of this binding site abolishes their miR‐490 responsiveness. Post‐transcriptional CCAT1 silencing by miR‐490 significantly suppressed GC cell migration. Furthermore, miR‐490 directly bound to the hnRNPA1 mRNA 3′‐UTR to repress its translation. Inhibition of miR‐490 rescued CCAT1 siRNA‐mediated suppression of cell migration. hnRNPA1 expression was significantly upregulated in GC specimens, and there was a negative correlation between miR‐490 and hnRNPA1 expression and also a positive correlation between hnRNAP1 expression level and CCAT1 level. Taken together, we show for the first time that the CCAT1/miR‐490/hnRNPA1 axis promotes GC migration, and it may have a possible diagnostic and therapeutic potential in GC. © 2016 IUBMB Life, 68(3):201–210, 2016