Novel interactions of vitamin E and estrogen in breast cancer

• Published in: Nutrition and cancer 2005-01, Vol.52 (1), p.43-48
• Main Authors: Chamras, H, Barsky, S.H, Ardashian, A, Navasartian, D, Heber, D, Glaspy, J.A
• Format: Article
• Language: English
• Subjects: alpha-tocopherol; alpha-Tocopherol - administration & dosage; alpha-Tocopherol - pharmacology; Antineoplastic Agents, Hormonal - antagonists & inhibitors; Biological and medical sciences; breast neoplasms; Breast Neoplasms - epidemiology; Breast Neoplasms - metabolism; Breast Neoplasms - prevention & control; Cell Division - drug effects; cell proliferation; clinical trials; Dietary Supplements; dosage; dose response; Dose-Response Relationship, Drug; Epidemiology; estrogens; Estrogens - metabolism; Female; Gynecology. Andrology. Obstetrics; hormone receptors; Humans; Mammary gland diseases; Medical sciences; nutritional intervention; Other treatments; Receptors, Estrogen - metabolism; Tamoxifen - antagonists & inhibitors; Treatment. General aspects; Tumor Cells, Cultured; Tumors; Vitamin E - administration & dosage; Vitamin E - pharmacology; vitamin supplements; Vitamins - administration & dosage; Vitamins - pharmacology
• ISSN: 0163-5581; 1532-7914
• DOI: 10.1207/s15327914nc5201_6

The prevention of breast cancer through dietary modification is an active area of clinical and epidemiological research. It has been proposed that dietary supplementation of vitamin E may reduce a woman's risk of developing breast cancer. However, the exact mechanism remains unknown. alpha-Tocopherol is the most biologically active form of vitamin E. We investigated the effect of vitamin E (alpha-tocopherol) on breast cancer cell growth. A dose-dependent inhibition of cell proliferation was found in estrogen receptor (ER)-positive cells showing a potent suppression of growth at 100 micromolar vitamin E in MCF-7 (53%) and T47D (75%) cells. Vitamin E reduced significantly the response of both cell lines to estrogen (10 nM), and cell proliferation was decreased in MCF-7 and T47D cells by 69% and 84%, respectively. No growth inhibition was observed when cells were grown in the absence of estrogen. Vitamin E altered and decreased the growth inhibition induced by tamoxifen (10 micromolar) in MCF-7 (33%) and T47D (54%) cells. In addition, the immunostaining of ER of MCF-7 cells was reduced by 30% in the presence of vitamin E, suggesting an effect of vitamin E on the expression of ER. This provides evidence that vitamin E may inhibit ER-positive cell growth by altering the cellular response to estrogen.