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MAPRE1 promotes cell cycle progression of hepatocellular carcinoma cells by interacting with CDK2.
Cell Biology International ( IF 3.3 ) Pub Date : 2020-08-08 , DOI: 10.1002/cbin.11442
Xing-Hua Liang 1 , Zheng-Ping Feng 1 , Fo-Qiu Liu 1 , Rong Yan 1 , Liang-Yu Yin 1 , Hao Shen 1 , Hai-Lin Lu 1
Affiliation  

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.

中文翻译:

MAPRE1通过与CDK2相互作用来促进肝癌细胞的细胞周期进程。

靶向细胞周期蛋白依赖性激酶(CDK)是一种有前途的癌症治疗方法。不幸的是,CDK抑制剂在肝细胞癌(HCC)中的疗效有限,部分原因是对细胞周期进程的不完全了解以及缺乏特定的生物标志物,无法充分识别哪些患者可能对CDK抑制剂有反应。在本研究中,我们报告微管相关蛋白RP / EB家族成员1(MAPRE1),一个参与细胞周期和微管调控的基因,在肝癌组织中显着增加,促进肝癌细胞增殖,增强体外肿瘤发生,并且与肝癌预后不良有关。我们证明,MAPRE1与CDK2结合,导致HCC细胞中CDK2 Thr161残基的过度磷酸化。
更新日期:2020-10-13
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