Mutant ACTB mRNA 3′-UTR promotes hepatocellular carcinoma development by regulating miR-1 and miR-29a

In recent years, studies demonstrate that ACTB has been found to be associated with various tumors. Although ACTB is dysregulated in numerous cancer types, limited data are available on the potential function and mechanism of ACTB in hepatocellular carcinoma (HCC). This study evaluated the expressio...

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Veröffentlicht in:Cellular signalling 2020-03, Vol.67, p.109479-109479, Article 109479
Hauptverfasser: Li, Yong, Ma, Hongbin, Shi, Changying, Feng, Feiling, Yang, Liang
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Sprache:eng
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Zusammenfassung:In recent years, studies demonstrate that ACTB has been found to be associated with various tumors. Although ACTB is dysregulated in numerous cancer types, limited data are available on the potential function and mechanism of ACTB in hepatocellular carcinoma (HCC). This study evaluated the expression and biological roles of mutant ACTB mRNA 3′-UTR in HCC. Transcriptome sequence and qRT-PCR analysis determined that mutant ACTB mRNA ′-UTR was high expression in tumor tissues. Luciferase reporter assay showed that the ACTB mRNA 3′-UTR mutations made it easier to interact with miR-1 and miR-29a. Moreover, mutant ACTB mRNA ′-UTR regulated miR-1 and miR-29a degradation via AGO2. Furthermore, mutant ACTB mRNA 3′-UTR promoted hepatocellular carcinoma cells migration and invasion in vitro and in vivo by up-regulating miR-1 target gene MET and miR-29a target gene MCL1. In a word, our study demonstrates that 3′-UTR of ACTB plays a key role in the development of hepatocellular carcinoma (HCC) and highlights the molecular mechanisms underlying such a complex process. •Mutant ACTB mRNA 3′UTR plays a key role in hepatocellular carcinoma development.•Mutant ACTB mRNA 3′UTR promoted hepatocellular carcinoma cells proliferation and migration in vitro and in vivo.•Mutant ACTB mRNA 3′UTR promoted hepatocellular cancer tumorigenesis by regulating miR-1 and miR-29a degradation via AGO2.
ISSN:0898-6568
1873-3913
DOI:10.1016/j.cellsig.2019.109479