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MAPRE1 promotes cell cycle progression of hepatocellular carcinoma cells by interacting with CDK2
Author(s) -
Liang Xinghua,
Feng Zhengping,
Liu Foqiu,
Yan Rong,
Yin Liangyu,
Shen Hao,
Lu Hailin
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11442
Subject(s) - cyclin dependent kinase , cancer research , cyclin dependent kinase 2 , cell cycle , cdk inhibitor , hepatocellular carcinoma , carcinogenesis , biology , kinase , hyperphosphorylation , cell growth , cyclin dependent kinase 1 , cell , cancer , microbiology and biotechnology , biochemistry , genetics
Targeting cyclin‐dependent kinases (CDKs) is a promising method of therapy for cancer. Unfortunately, the efficacy of CDK inhibitors in hepatocellular carcinoma (HCC) is limited, due in part to incomplete understanding of cell cycle progression and a lack of specific biomarkers to adequately identify which patients may be responsive to CDK inhibitors. In the present study, we report that microtubule‐associated protein RP/EB family member 1 (MAPRE1), a gene involved in cell cycle and microtubule regulation, is significantly increased in HCC tissue, promotes HCC cell proliferation, enhances in vitro tumorigenesis, and associates with poor prognosis of HCC. We demonstrate that MAPRE1 binds with CDK2, resulting in the hyperphosphorylation of the CDK2 Thr161 residue in HCC cells. Our findings reveal that targeting MAPRE1 might be an effective therapeutic strategy in HCC, and suggest that MAPRE1 expression might provide a promising biomarker to stratify patients with HCC who may benefit from treatment with CDK inhibitors.