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首页> 外文期刊>Glycoconjugate Journal >α1,3 Fucosyltransferase-VII modifies the susceptibility of apoptosis induced by ultraviolet and retinoic acid in human hepatocarcinoma cells
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α1,3 Fucosyltransferase-VII modifies the susceptibility of apoptosis induced by ultraviolet and retinoic acid in human hepatocarcinoma cells

机译:α1,3岩藻糖基转移酶-VII改变紫外线和视黄酸诱导的人肝癌细胞凋亡的敏感性

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摘要

The role of α1,3fucosyltransferase-VII (α1,3 FucT-VII) in cell apoptosis was studied in human hepatocellular carcinoma H7721 cells. After the cells were transfected with α1,3 FucT-VII cDNA, the expression of apoptotic protease, procaspase-3, was decreased, while the anti-apoptotic proteins, phospho-PKB and phospho-Bad were increased as compared with mock (vector) transfected cells, indicating that α1,3FucT-VII is a potential anti-apoptotic factor in H7721 cells. After “α1,3FucT-VII” cells were irradiated by UV to induce apoptosis, the anti-apoptotic potential of α1,3FucT-VII became more apparent, as evidenced by the less apoptotic cell % and active cleaved caspase-3, more phospho-p38 MAPK and JNK (two anti-apoptotic signaling molecules in H7721 cells responsible to UV stress) when compared with the “Mock” cells. In contrast, “α1,3FucT-VII” cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-XL. The up regulation of α1,3FucT-VII mRNA and cell surface SLex (α1,3FucT-VII product) by UV and down regulation of them by ATRA was speculated to be one of the mechanisms that α1,3FucT-VII decreased and increased the susceptibility of apoptosis induced by UV and ATRA respectively.
机译:研究了人类肝细胞癌H7721细胞中α1,3岩藻糖基转移酶VII(α1,3FucT-VII)在细胞凋亡中的作用。与模拟载体相比,用α1,3FucT-VII cDNA转染细胞后,凋亡蛋白酶procaspase-3的表达降低,而抗凋亡蛋白磷酸化PKB和磷酸化Bad升高。转染的细胞,表明α1,3FucT-VII是H7721细胞中潜在的抗凋亡因子。在用紫外线照射“α1,3FucT-VII”细胞以诱导凋亡后,α1,3FucT-VII的抗凋亡潜力变得更加明显,这是由凋亡细胞百分比降低和活性裂解的caspase-3减少所证明,磷酸化程度更高。与“模拟”细胞相比,p38 MAPK和JNK(H7721细胞中两个抗凋亡信号分子负责紫外线胁迫)。相比之下,“α1,3FucT-VII”细胞促进了全反式维甲酸(ATRA)诱导的凋亡,这在流式细胞仪分析中更大的sub-G1(凋亡细胞)峰得到证实,活性半胱天冬酶- 3和促凋亡蛋白Bax,以及抗凋亡蛋白Bcl-2和Bcl-XL的表达较少。紫外线对α1,3FucT-VIImRNA和细胞表面SLex (α1,3FucT-VII产物)的上调以及ATRA对它们的下调被认为是α1,3FucT-VII降低的机制之一分别增加了紫外线和ATRA诱导的细胞凋亡敏感性。

著录项

  • 来源
    《Glycoconjugate Journal》 |2007年第5期|207-220|共14页
  • 作者单位

    Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College Fudan University Shanghai 200032 People’s Republic of China;

    Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College Fudan University Shanghai 200032 People’s Republic of China;

    Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College Fudan University Shanghai 200032 People’s Republic of China;

    Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College Fudan University Shanghai 200032 People’s Republic of China;

    Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College Fudan University Shanghai 200032 People’s Republic of China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Human hepatocarcinoma cell line; α1; 3 Fucosyltransferase-VII; Apoptosis; Mitochondria pathway; p38 MAPK/JNK pathways;

    机译:人肝癌细胞系;α1;3岩藻糖基转移酶-VII;凋亡;线粒体途径;p38 MAPK / JNK途径;

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