Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A. Issue 11 (12th November 2019)

• Record Type: Journal Article
• Authors: He, Jinyu; Yu, Jiao
• Is Part Of: Bioscience reports. Volume 39:Issue 11(2019)
• Publication Date: 2019-11-12
• Subjects: FAM83A-AS1 -- FAM83A -- hepatocellular carcinoma -- NOP58; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20192550
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract: Hepatocellular carcinoma (HCC), as one of the commonest cancers globally, is a primary malignancy in human liver with a characteristic of high mortality rate. Long noncoding RNAs (lncRNAs) are confirmed to be implicated with multiple cancers including HCC. LncRNA FAM83A-AS1 has also been validated as an oncogene in lung cancer, but its mechanism in HCC is poorly understood. Our research is intended to investigate the underlying mechanism of FAM83A-AS1 in HCC. In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells. FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC. Moreover, FAM83A-AS1 could positively regulate FAM83A, and FAM83A could also promote the progression of HCC. In addition, FAM83A-AS1 and FAM83A were both verified to bind with NOP58, and FAM83A-AS1 enhanced the mRNA stability of FAM83A by binding with NOP58. In rescue assays, the suppressed influence of down-regulated FAM83A-AS1#1 on cell proliferation, migration as well as the accelerated influence of FAM83A-AS1#1 knockdown on cell apoptosis could be partially recovered by overexpression of FAM83A. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM83A. These findings offer a novel biological insight into HCC treatment.