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and ERß Is Associated with Estrogen-mediated Modulation of Intestinal Tumorigenesis1
Departments of Surgery and Pathology, Weill College of Medicine of Cornell University, New York, New York [M. J. W., A. M. C., N. N. M., H. R., R. T. B.]; Division of Surgical Oncology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115 [M. M. B.]; and The Strang Cancer Prevention Center, New York, New York 10021 [M. J. W., A. M. C., N. N. M., H. L. B., M. M. B.]
Menopausal hormone replacement therapy has been widely used to alleviate the symptoms of menopause and to decrease the detrimental effects of ovarian hormone loss on bone density and cardiovascular health. Multiple studies of colorectal cancer epidemiology also support a role for hormone replacement therapy in prevention of colorectal cancer. We studied the effect of ovariectomy and estrogen replacement on tumor formation in C57BL/6J-Min/+ (Min/+) mice, animals that bear a germ-line mutation in murine Apc. These mice develop multiple intestinal tumors that show loss of wild-type Apc protein. After ovariectomy, intestinal adenomas in Min/+ mice increased by 77% (P = 0.0004). Ovariectomized Min/+ mice that were treated with a replacement dose of 17ß-estradiol had the same number of tumors as Min/+ mice that were neither castrated nor treated with estrogen replacement (P = 0.85). Examination of estrogen receptor (ER) levels in intestinal tissue by immunoblot showed changes in relative expression levels of ER
and ERß, with highest ER and lowest ERß expression in the normal-appearing intestine of Min/+ mice, and lowest ER and highest ERß expression in the enterocytes of animals that received 17ß-estradiol. These results suggest that endogenous estrogens protect against Apc-associated tumor formation and that tumor prevention by 17ß-estradiol is associated with an increase in ERß and a decrease in ER expression in the target tissue.
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