Journal
JOURNAL OF UROLOGY
Volume 168, Issue 4, Pages 1578-1582Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/S0022-5347(05)64524-7
Keywords
prostate; prostatic neoplasms; antioxidants; vitamin E; cell cycle
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Purpose: Vitamin E has been identified as a candidate agent for the prevention of prostate cancer. We hypothesize that the mechanism for this effect is in part a result of cell cycle inhibition rather than only due to a reduction in reactive oxygen species. We tested whether vitamin K induces cell cycle arrest in prostate carcinoma, mediated by alterations in cell cycle regulatory proteins, including cyclin E, cdk2 and p27. Materials and Methods: Cells were incubated with and without vitamin E (alpha-tocopherol succinate, 20 mug./ml.), fixed and stained with propidium. iodide for flow cytometry analysis. In parallel experiments total protein was extracted, immunoprecipitated with cyclin E antibody and analyzed by Western blot for the expression of cell cycle markers. Results: Flow cytometry analysis revealed a dramatic reduction in the S phase percent of LNCaP and PC3 cells in response to vitamin E (69% and 95%, respectively). It was accompanied by over expression of p27 (3-fold increase) with vitamin E treatment. Conclusions: This study demonstrates that at physiological concentrations vitamin E induced profound cell cycle arrest mediated by up-regulation of p27. This observation provides a theoretical basis for the putative chemopreventive effect of vitamin E.
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