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论文题目: Triosephosphate isomerase 1 suppresses growth, migration and invasion of hepatocellular carcinoma cells
英文论文题目: Triosephosphate isomerase 1 suppresses growth, migration and invasion of hepatocellular carcinoma cells
第一作者: Jiang, H; Ma, N; Shang, YR; Zhou, WT; Chen, TW; Guan, DX; Li, JJ; Wang, JJ; Zhang, EB; Feng, YY; Yin, FF; Yuan, YM; Fang, YY; Qiu, L; Xie, D; Wei, DZ
英文第一作者: Jiang, H; Ma, N; Shang, YR; Zhou, WT; Chen, TW; Guan, DX; Li, JJ; Wang, JJ; Zhang, EB; Feng, YY; Yin, FF; Yuan, YM; Fang, YY; Qiu, L; Xie, D; Wei, DZ
联系作者: Xie, D (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, 320 Yueyang Rd, Shanghai 200031, Peoples R China.
英文联系作者: Xie, D (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, 320 Yueyang Rd, Shanghai 200031, Peoples R China.
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发表年度: 2017
卷: 482
期: 4
页码: 1048-1053
摘要: Metabolic dysregulation is one of the most common and recognizable features of cancer. Triosephosphate isomerase 1 (TPI1), which catalyzes the interconversion of dihydroxyacetone phosphate (DHAP) and D-glyceraldehyde-3-phosphate (G3P) during giycosis and gluconeogenesis, is a crucial enzyme in the carbohydrate metabolism. However, the biological function and mechanism of TPI1 in cancer remain largely unknown. In this study, we have found that TPI1 expression was greatly decreased in clinical HCC samples, positively correlated with overall survival, and negatively associated with histological differentiation, tumor size and organ metastasis. Forced expression of TPI1 in HCC cells inhibited cell growth, migration, and invasion in vitro. Consistently, knockdown of TPI1 by shRNA promoted cell growth, migration and invasion. Moreover, overexpression of TPI1 led to slowed tumor growth and decreased tumor weight in vivo. Furthermore, cell cycle arrest was induced by TPI1 over expression. These phenotypes were associated with altered expression of beta-catenin, Vimentin, P53, P27 and CyclinD1. Therefore, our data suggested that TPI1 functioned as a tumor suppressor in HCC and might serve as a potential therapeutic target for the treatment of HCC.
英文摘要: Metabolic dysregulation is one of the most common and recognizable features of cancer. Triosephosphate isomerase 1 (TPI1), which catalyzes the interconversion of dihydroxyacetone phosphate (DHAP) and D-glyceraldehyde-3-phosphate (G3P) during giycosis and gluconeogenesis, is a crucial enzyme in the carbohydrate metabolism. However, the biological function and mechanism of TPI1 in cancer remain largely unknown. In this study, we have found that TPI1 expression was greatly decreased in clinical HCC samples, positively correlated with overall survival, and negatively associated with histological differentiation, tumor size and organ metastasis. Forced expression of TPI1 in HCC cells inhibited cell growth, migration, and invasion in vitro. Consistently, knockdown of TPI1 by shRNA promoted cell growth, migration and invasion. Moreover, overexpression of TPI1 led to slowed tumor growth and decreased tumor weight in vivo. Furthermore, cell cycle arrest was induced by TPI1 over expression. These phenotypes were associated with altered expression of beta-catenin, Vimentin, P53, P27 and CyclinD1. Therefore, our data suggested that TPI1 functioned as a tumor suppressor in HCC and might serve as a potential therapeutic target for the treatment of HCC.
刊物名称: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
英文刊物名称: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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学科: Biochemistry & Molecular Biology; Biophysics
英文学科: Biochemistry & Molecular Biology; Biophysics
影响因子: 2.466
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论文类别: Article
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