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Journal of Environmental Pathology, Toxicology and Oncology
Fator do impacto: 1.625 FI de cinco anos: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Imprimir: 0731-8898
ISSN On-line: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i3.30
9 pages

Vanadate Induces G2/M Phase Arrest in p53-Deficient Mouse Embryo Fibroblasts

Zhuo Zhang
Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, KY
Fei Chen
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown,WV
Chuanshu Huang
New York University,Nelson Institute of Environment Medicine, New York University School of Medicine, New York, NY 10061
Xianglin Shi
Division of Nutritional Sciences, Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, KY; Center for Research on Environmental Disease, College of Medicine, University of Kentucky, Lexington, KY; Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, KY

RESUMO

Vanadium compounds exert potent toxic and carcinogenic effects on a wide variety of biological systems. The mechanisms involved in their toxicity and carcinogenesis require investigation. Cell growth arrest and its regulation are important mechanisms in maintaining genomic stability and integrity in response to environmental stress. The p53 tumor suppressor plays a central role in the regulation of the normal cell cycle. To investigate the role ofp53 in vanadate-induced cell growth arrest and its regulation, two cell lines— normal mouse embryo fibroblasts [p53(+/+)] and p53-deficient mouse embryo fibroblasts [p53(-/-)],— were used in this study. Flow cytometry was used to analyze cell growth arrest at G0/G1, S, or G2/M phase. Western blotting analysis was performed to determine several cell growth regulatory proteins. The results showed that in p53(-/-) cells vanadate induced G2/M phase arrest in a dose- and time-dependent manner without alteration of S phase. In p53(+/+) cells, vanadate treatment increased the S phase with no significant change in the G2/M phase. Furthermore, Western blotting results showed that in p53(-/-) cells vanadate caused cdc25C degradation and activation ofphospho-cdc2 without alteration of the p21 level. In p53(+/+) cells, vanadate increased the expression of p21 and degraded cdc25A instead of cdc25C without any effect on cdc2. These results demonstrate that vanadate induced G2/M phase arrest in p53-deficient mouse embryo fibroblasts, and promoted S phase entry in p53 wild-type mouse embryo fibroblasts.


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