Literature DB >> 23466643

miR-371-5p down-regulates pre mRNA processing factor 4 homolog B (PRPF4B) and facilitates the G1/S transition in human hepatocellular carcinoma cells.

Rui-Yan Liu1, Cai-Feng Diao, Yi Zhang, Nan Wu, Hai-Ying Wan, Xiang-Yang Nong, Min Liu, Hua Tang.   

Abstract

Increasing evidence has lent support to the notion that miRNAs regulate hepatocellular carcinoma (HCC) cell proliferation by directly targeting cell cycle-related genes. Among these genes, we identified PRPF4B, a CDK-like kinase, as a new target of miR-371-5p. Over-expression of miR-371-5p and knockdown of PRPF4B promotes cell growth by accelerating the G1/S transition in HCC cell lines. Moreover, miR-371-5p promotes tumor growth of QGY-7703 cells in vivo. Conversely, inhibition of miR-371-5p yields an opposing effect. Ectopic expression of PFPF4B abolishes the malignant phenotypes caused by miR-371-5p. Furthermore, contrary to PRPF4B, miR-371 was up-regulated in HCC tissues. Collectively, we highlight the significance of miR-371-5p and PRPF4B in cell cycle progression and hepatocarcinogenesis.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

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Year:  2013        PMID: 23466643     DOI: 10.1016/j.canlet.2013.02.045

Source DB:  PubMed          Journal:  Cancer Lett        ISSN: 0304-3835            Impact factor:   8.679


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