Prohibitin-2 promotes hepatocellular carcinoma malignancy progression in hypoxia based on a label-free quantitative proteomics strategy

文献类型： 外文期刊

第一作者： Cheng, Jun

作者： Cheng, Jun;Wu, Jian;Wu, Liming;Xie, Haiyang;Zheng, Shusen;Zhou, Lin;Cheng, Jun;Gao, Feng;Xing, Chunyang;Lv, Zhen;Wu, Liming;Ye, Sunyi;Xie, Haiyang;Zheng, Shusen;Zhou, Lin;Gao, Feng;Chen, Xiang;Xu, Wei;Xie, Qing

作者机构：

关键词： Biomarker;Hepatocellular carcinoma;Label-free;Prohibitin-2;Proteomics

期刊名称：MOLECULAR CARCINOGENESIS （ 影响因子：4.784； 五年影响因子：4.385 ）

ISSN：

年卷期：

页码：

收录情况： SCI

摘要： The rapid growth of hepatocellular carcinoma (HCC) leading to tumor hypoxia is a common pathological phenomenon. Meanwhile, tumor hypoxia can promote a change in the biological properties of tumor cells. It may enhance the survival of tumor cells under stress conditions, resulting in resistance to apoptosis and angiogenesis. The moleculars that could modulate the malignant phenotypes of HCC cells remain largely unknown. Based on label-free quantitative proteomic data, we found a significant upregulation of prohibitin-2 (PHB2) in HCC tissues. Treatment of hepatoma cells with small interfering RNAs against PHB2 suppressed cell growth and colony formation, led to G1 phase arrest and sensitized HCC cells to apoptosis. Moreover, inhibition of PHB2 expression dramatically repressed the ability of HCC cells to adapt to hypoxic microenvironments and resist chemotherapy-induced apoptosis. Thus, PHB2 in HCC supports the development and progression of hepatocellular malignancy to hypoxia, and implicates the potential antagonist function of PHB2 in transarterial chemoembolization treatment.

分类号： R73

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