| Literature DB >> 31837982 |
Shiji Fang1, Dengke Zhang1, Wei Weng1, Xiuling Lv1, Liyun Zheng2, Minjiang Chen1, Xiaoxi Fan1, Jianting Mao1, Chenchen Mao1, Yani Ye1, Min Xu3, Jiansong Ji4.
Abstract
Alternative splicing within a gene can create different versions of an mRNA, called isoforms. CFIm, composed of a small subunit CFIm25 and two large subunits CFIm68 and CFIm59 (also known as CPSF7), has been proposed as an enhancer-dependent activator of mRNA 3' processing. In this study, we investigated the role of CPSF7 in hepatocellular carcinoma. Experimental evidence suggests that the expression level of CPSF7 is higher in liver cancer cells and tissues than in non-tumor hepatic cells and tissues. Furthermore, knockdown of CPSF7 effectively suppressed cell proliferation, migration and colony formation in liver cancer cells by inhibiting PTEN/AKT signaling. CPSF7 promoted WWP2-FL due to the presence of PTEN ubiquitination sites in this longer transcript. Taken together, we identified that CPSF7 regulates liver cancer growth by targeting WWP2-FL that in turn regulates AKT activation in a PTEN-dependent manner.Entities:
Keywords: Alternative polyadenylation; CPSF7; Hepatocellular carcinoma; PTEN/AKT signaling; WWP2
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Year: 2019 PMID: 31837982 DOI: 10.1016/j.bbamcr.2019.118624
Source DB: PubMed Journal: Biochim Biophys Acta Mol Cell Res ISSN: 0167-4889 Impact factor: 4.739