Journal article
Radiosensitizing and anti-proliferative effects of resveratrol in two human cervical tumor cell lines
Cancer letters, Vol.175(2), pp.165-173
2002
DOI: 10.1016/S0304-3835(01)00719-4
PMID: 11741744
Abstract
Resveratrol is a polyphenol isolated from the skins of grapes that has been shown to significantly alter the cellular physiology of tumor cells, as well as block the process of initiation and progression. At least one mechanism for the intracellular actions of resveratrol involves the suppression of prostaglandin (PG) biosynthesis. The involvement of PGs and other eicosanoids in the development of human cancer is well established. PGs are synthesized from arachidonic acid via the cyclooxygenase pathway and have multiple physiological and pathological functions. In addition, evidence has arisen suggesting that PGs may be implicated in the cytotoxic and/or cytoprotective response of tumor cells to ionizing radiation (IR). As such, we hypothesized that tumor cells may exhibit changes in the cellular response to IR following exposure to resveratrol, a naturally occuring compound that inhibits cyclooxygenase-1 (COX-1) activity. Thus, clonogenic cell survival assays were performed using irradiated HeLa and SiHa cells pretreated with resveratrol prior to IR exposure, and resulted in enhanced tumor cell killing by IR in a dose-dependent manner. Further analysis of COX-1 inhibition indicated that resveratrol pretreatment: (1), inhibited cell division as assayed by growth curves; and (2), induced an early S phase cell cycle checkpoint arrest, as demonstrated by fluorescence-activated cell sorting, as well as bromodeoxyuridine pulse-chase analysis. These results suggest that resveratrol alters both cell cycle progression and the cytotoxic response to IR in two cervical tumor cell lines.
Details
- Title: Subtitle
- Radiosensitizing and anti-proliferative effects of resveratrol in two human cervical tumor cell lines
- Creators
- Imran Zoberi - Section of Cancer Biology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USAC.Matthew Bradbury - Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 10 Room B3B69, Bethesda, MD 20892-1002301, USAHeather A Curry - Section of Cancer Biology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USAKheem S Bisht - Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 10 Room B3B69, Bethesda, MD 20892-1002301, USAPrabhat C Goswami - Free Radical and Radiation Biology Program, Department of Radiation Oncology, B180 Medical Laboratories, University of Iowa, Iowa City, IA 52242, USAJoseph L Roti Roti - Section of Cancer Biology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, USADavid Gius - Radiation Oncology Branch, Radiation Oncology Sciences Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 10 Room B3B69, Bethesda, MD 20892-1002301, USA
- Resource Type
- Journal article
- Publication Details
- Cancer letters, Vol.175(2), pp.165-173
- Publisher
- Elsevier Ireland Ltd
- DOI
- 10.1016/S0304-3835(01)00719-4
- PMID
- 11741744
- ISSN
- 0304-3835
- eISSN
- 1872-7980
- Language
- English
- Date published
- 2002
- Academic Unit
- Radiation Oncology
- Record Identifier
- 9984047719002771
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