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UBAP2 negatively regulates the invasion of hepatocellular carcinoma cell by ubiquitinating and degradating Annexin A2

机译:UBAP2通过泛素化和降解膜联蛋白A2负调节肝细胞癌细胞的侵袭

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摘要

The ubiquitin-dependent proteasomal degradation of proteins controls signaling and cellular survival. In this study, we found that ubiquitin associated protein 2 (UBAP2) was significantly downregulated in hepatocellular carcinoma (HCC) tissues compared with adjacent normal tissues. Furthermore, higher expression of UBAP2 in cancer tissues was correlated with good prognosis in HCC patients. Knockdown of UBAP2 significantly enhanced the invasion and proliferation of HCC cells in vitro and promoted tumor growth in vivo, while enforced expression of UBAP2 impaired the aggressive ability and tumor growth of HCC cells. Mechanistically, UBAP2 formed a complex with Annexin A2 and promoted the degradation of Annexin A2 protein by ubiquitination, and then inhibited HCC progression. Collectively, UBAP2 appears as a novel marker for predicting prognosis and a therapeutic target for HCC.
机译:蛋白质的泛素依赖性蛋白酶体降解控制信号传导和细胞存活。在这项研究中,我们发现与邻近的正常组织相比,肝细胞癌(HCC)组织中的泛素相关蛋白2(UBAP2)明显下调。此外,在癌组织中UBAP2的高表达与HCC患者的良好预后相关。敲低UBAP2显着增强了体外HCC细胞的侵袭和增殖,并促进了体内肿瘤的生长,而UBAP2的强制表达削弱了HCC细胞的侵袭能力和肿瘤生长。从机理上讲,UBAP2与膜联蛋白A2形成复合物,并通过泛素化促进膜联蛋白A2蛋白的降解,然后抑制HCC进程。 UBAP2集体表现为预测HCC预后的新标志物和治疗靶标。

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