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Cyclin A is essential for the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells
Wang, Zhiqin1,3; Qi, Yitao1; Chen, Qian1; Yang, Di1; Tang, Shusheng1; Jin, Xi1; Gao, Jie1; Fu, Juanling2; Zhou, Zongcan2; Wang, Jie3; Xiao, Xilong1
关键词P53 Benzo(a)Pyrene Cell Cycle Cyclin a
刊名TOXICOLOGY
2009-02-04
DOI10.1016/j.tox.2008.10.018
256期:1-2页:1-6
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]Pharmacology & Pharmacy ; Toxicology
关键词[WOS]LUNG-CANCER CELLS ; DNA-DAMAGE ; S-PHASE ; GROWTH ARREST ; G(1) ARREST ; P53 ; EXPRESSION ; APOPTOSIS ; FIBROBLASTS ; INDUCTION
英文摘要

Benzo(a)pyrene (B(a)P) is an environment carcinogen that can enhance cell proliferation by disturbing the signal transduction pathways in cell cycle regulation. The p53 tumor suppressor as a cell cycle check-point determinant plays a critical role in cell proliferation. However, the mechanism of p53 that accounts for the remarkable toxicity of B(a)P remains elusive. Here we reported that exposure of B(a)P to A549 cells caused G1 to S and G2/M phase transition along with increased expression of p53, cyclin D1, Cdk2, Cdk4, p21 and decreased expression of cyclin E, but no change in cyclin A and p27 expression. Up-regulation of p53 expression via transfection caused G1 phase arrest with decreased expression of cyclin A, E, Cdk2 and Cdk4, and increased expression of p21, when the expression of cyclin D1 and p27 were not significant changed. While B(a)P exposure to A549 cells following p53 transfection. up-regulation of p53 significantly attenuated the B(a)P-induced enhancement of cell proliferation and cell arrest, with increased expression of cyclin D1, Cdk2 and Cdk4, and with declined expression of cyclin A, cyclin E and p21, and p27 were not significant changed. Compared to the untreated cells, cylin A expression reduced in p53-transfected cells and in the B(a)P-treated cells following p53 transfection, but showed no change in the only B(a)P-treated cells. These results indicated that cyclin A is regulated by p53, not by B(a)P, and it is essential in the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells, cyclin E and p21 also as downstream genes of p53 involved it, which is p27-independent. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000263218300001
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/58036
专题北京大学公共卫生学院_毒理学系
北京大学公共卫生学院_公共卫生学院
作者单位1.China Agr Univ, Coll Vet Med, Dept Pharmacol & Toxicol, Beijing 100094, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Toxicol, Beijing 100083, Peoples R China
3.Natl Shenyang New Drug Evaluat Ctr, Chem & Ind Res Inst, Shenyang 110021, Peoples R China
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Wang, Zhiqin,Qi, Yitao,Chen, Qian,et al. Cyclin A is essential for the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells[J]. TOXICOLOGY,2009,256(1-2):1-6.
APA Wang, Zhiqin.,Qi, Yitao.,Chen, Qian.,Yang, Di.,Tang, Shusheng.,...&Xiao, Xilong.(2009).Cyclin A is essential for the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells.TOXICOLOGY,256(1-2),1-6.
MLA Wang, Zhiqin,et al."Cyclin A is essential for the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells".TOXICOLOGY 256.1-2(2009):1-6.
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