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17 beta-Oestradiol attenuates nucleotide excision repair
Mark D Evans1, John M Butler, Karen Nicoll
1Oxidative Stress Group, Department of Clinical Biochemistry, P.O. Box 65, Robert Kilpatrick Clinical Sciences Building, University of Leicester, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LE2 7LX, UK. mde2@le.ac.uk
FEBS Letters
|February 1, 2003
Summary
Chronic exposure to 17 beta-estradiol (E2) may increase cancer risk by inhibiting DNA repair. This study shows E2 treatment reduces the removal of UV-induced DNA damage in human cells.
Area of Science:
- Endocrinology
- Molecular Biology
- Cancer Research
Background:
- Epidemiological studies link chronic endogenous estrogen exposure to breast and gynecological tumors.
- 17 beta-estradiol (E2) is implicated in tumorigenesis via cell proliferation and genotoxic metabolite production.
Purpose of the Study:
- To investigate the potential role of 17 beta-estradiol (E2) in inhibiting DNA repair mechanisms.
- To explore a novel mechanism contributing to E2's carcinogenic potential.
Main Methods:
- Human keratinocytes were treated with 17 beta-estradiol (E2).
- The removal of UV-induced thymine dimers, a measure of nucleotide excision repair, was assessed.
- The effect of 17 alpha-estradiol was evaluated for comparison.
Main Results:
- Treatment with E2 significantly attenuated the removal of UV-induced thymine dimers in keratinocytes.
- 17 alpha-estradiol did not exhibit this inhibitory effect on DNA repair.
- This suggests E2 actively interferes with DNA repair processes.
Conclusions:
- 17 beta-estradiol (E2) may promote tumorigenesis by inhibiting DNA repair.
- This DNA repair inhibition represents an additional mechanism for E2's carcinogenic potential.
- Further research into E2's effects on DNA repair is warranted.