α1,3 Fucosyltransferase-VII modifies the susceptibility of apoptosis induced by ultraviolet and retinoic acid in human hepatocarcinoma cells

被引:1
作者
Hao Wang
Qiu-Yan Wang
Ying Zhang
Zong-Hou Shen
Hui-Li Chen
机构
[1] Fudan University,Key Laboratory of Glycoconjugate Research, Ministry of Health, Department of Biochemistry, Shanghai Medical College
来源
Glycoconjugate Journal | 2007年 / 24卷
关键词
Human hepatocarcinoma cell line; α1; 3 Fucosyltransferase-VII; Apoptosis; Mitochondria pathway; p38 MAPK/JNK pathways;
D O I
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学科分类号
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.
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页码:207 / 220
页数:13
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[1]  
Ashkenazi A.(19998)Death receptor signaling and modulation Science 281 1305-1308
[2]  
Dixit V.M.(2001)Mammalian mitogen-activated protein kinase signaling pathways activated by stress and inflammation Physiol. Rev. 81 807-869
[3]  
Kyriakis J.M.(1999)Signaling by germinal center kinase family of protein kinases J. Biol. Chem. 274 5258-5262
[4]  
Avruch J.(2002)Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases Science 298 1911-1912
[5]  
Kyriakis J.M.(2003)Mitochondrial control of apoptosis: an introduction Biochem. Biophys. Res. Commun. 304 433-435
[6]  
Johnson G.L.(2001)Life-or-death decisions by the Bcl-2 protein family Trends Biochem. Sci. 26 61-66
[7]  
Lapadat R.(2000)Bcl-2 family: life-or-death switch FEBS Lett. 466 6-10
[8]  
Kroemer G.(2003)Mechanisms of cytochrome c release by proapoptotic BCL-2 family members Biochem. Biophys. Res. Commun. 304 437-444
[9]  
Adams J.M.(2000)The Bcl-2 protein family Exp. Cell Res. 265 50-57
[10]  
Cory S.(1999)Mammalian caspases: structure, activation, substrates, and functions during apoptosis Ann. Rev. Biochem. 68 383-424