In Vitro Inhibition of Proliferation of Estrogen-Dependent and Estrogen-Independent Human Breast Cancer Cells Treated with Carotenoids or Retinoids
Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (β-carotene, canthaxanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, β-carotene significa...
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Published in | The Journal of nutrition Vol. 131; no. 5; pp. 1574 - 1580 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Elsevier Inc
01.05.2001
American Society for Nutritional Sciences American Institute of Nutrition |
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Abstract | Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (β-carotene, canthaxanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, β-carotene significantly reduced the growth of MCF-7 and Hs578T cells, and lycopene inhibited the growth of MCF-7 and MDA-MB-231 cells. Canthaxanthin did not affect the proliferation of any of the three cell lines. All-trans- and 9-cis-retinoic acid significantly reduced the growth of both MCF-7 and Hs578T cells, whereas 13-cis-retinoic acid and all-trans-retinol had a significant effect only on MCF-7 cells. MCF-7 and Hs578T cells treated with all-trans-retinoic acid (all-t-RA) were further studied for the mechanism behind growth inhibition. Retinoic acid receptors α and γ (RARα, γ) in MCF-7 cells and RARα, β and γ in Hs578T cells were not induced by all-t-RA treatment at either the protein or mRNA level. Hs578T cells treated with all-t-RA had significantly more cells in the G0/G1 stage of the cell cycle, but the same was not observed for MCF-7 cells. All-t-RA induced a dose-dependent cell death in MCF-7 cells, which may be a necrotic phenomenon. These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible. J. Nutr. 131: 1574–1580, 2001. |
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AbstractList | Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (beta-carotene, canthaxanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, beta-carotene significantly reduced the growth of MCF-7 and Hs578T cells, and lycopene inhibited the growth of MCF-7 and MDA-MB-231 cells. Canthaxanthin did not affect the proliferation of any of the three cell lines. All-trans- and 9-cis-retinoic acid significantly reduced the growth of both MCF-7 and Hs578T cells, whereas 13-cis-retinoic acid and all-trans-retinol had a significant effect only on MCF-7 cells. MCF-7 and Hs578T cells treated with all-trans-retinoic acid (all-t-RA) were further studied for the mechanism behind growth inhibition. Retinoic acid receptors alpha and gamma (RARalpha, gamma) in MCF-7 cells and RARalpha, beta and gamma in Hs578T cells were not induced by all-t-RA treatment at either the protein or mRNA level. Hs578T cells treated with all-t-RA had significantly more cells in the G0/G1 stage of the cell cycle, but the same was not observed for MCF-7 cells. All-t-RA induced a dose-dependent cell death in MCF-7 cells, which may be a necrotic phenomenon. These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible. Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (β-carotene, canthaxanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, β-carotene significantly reduced the growth of MCF-7 and Hs578T cells, and lycopene inhibited the growth of MCF-7 and MDA-MB-231 cells. Canthaxanthin did not affect the proliferation of any of the three cell lines. All-trans- and 9-cis-retinoic acid significantly reduced the growth of both MCF-7 and Hs578T cells, whereas 13-cis-retinoic acid and all-trans-retinol had a significant effect only on MCF-7 cells. MCF-7 and Hs578T cells treated with all-trans-retinoic acid (all-t-RA) were further studied for the mechanism behind growth inhibition. Retinoic acid receptors α and γ (RARα, γ) in MCF-7 cells and RARα, β and γ in Hs578T cells were not induced by all-t-RA treatment at either the protein or mRNA level. Hs578T cells treated with all-t-RA had significantly more cells in the G0/G1 stage of the cell cycle, but the same was not observed for MCF-7 cells. All-t-RA induced a dose-dependent cell death in MCF-7 cells, which may be a necrotic phenomenon. These results demonstrate that ER status is an important, although not essential factor for breast cancer cell response to carotenoid and retinoid treatments, and the mode of action of all-t-RA in MCF-7 and Hs578T cells is not through the induction of RAR. Other mechanistic pathways that are either followed by or concomitant with growth inhibition are possible. J. Nutr. 131: 1574–1580, 2001. Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (beta-carotene, canthazanthin and lycopene) and retinoids (all-trans-, 9-cis- and 13-cis-retinoic acid and all-trans-retinol). Among carotenoids, beta-carotene significanly reduced the growth of MCF-7 and Hs578T cells, and lycopene inhibited the growth of MCF-7 and MDA-MB-231 cells. |
Author | Krinsky, Norman I. Russell, Robert M. Prakash, Pankaj |
Author_xml | – sequence: 1 givenname: Pankaj surname: Prakash fullname: Prakash, Pankaj email: pankaj@silicoinsights.com organization: Department of Biochemistry, School of Medicine, Tufts University, Boston, MA 02111-1837 – sequence: 2 givenname: Robert M. surname: Russell fullname: Russell, Robert M. organization: Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111-1837 – sequence: 3 givenname: Norman I. surname: Krinsky fullname: Krinsky, Norman I. organization: Department of Biochemistry, School of Medicine, Tufts University, Boston, MA 02111-1837 |
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Keywords | breast cancer cells retinoic acid RAR THF ER(−) cell cycle β-carotene all-t-RA retinoic acid receptors ER(+) RXR Human Cell proliferation Cell culture Retinoid Anticarcinogen Gene expression Feeding Micronutrient Cell line Mammary gland Inhibition Carotenoid Tumor cell Biological receptor |
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Snippet | Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (β-carotene,... Both estrogen-receptor (ER) positive MCF-7 and ER-negative Hs578T and MDA-MB-231 human breast cancer cells were treated with carotenoids (beta-carotene,... |
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SubjectTerms | Antioxidants - pharmacology Apoptosis - drug effects Biological and medical sciences Blotting, Northern Breast cancer breast cancer cells Breast Neoplasms - drug therapy Canthaxanthin - therapeutic use Carcinogenesis, carcinogens and anticarcinogens Carotenoids - therapeutic use cell cycle Cell Division - drug effects Cells Female Fetuses Flow Cytometry Foods and miscellaneous Hormones Humans Medical sciences Receptors, Estrogen - drug effects retinoic acid retinoic acid receptors Retinoids - therapeutic use Tumor Cells, Cultured - drug effects Tumors Vitamin A β-carotene |
Title | In Vitro Inhibition of Proliferation of Estrogen-Dependent and Estrogen-Independent Human Breast Cancer Cells Treated with Carotenoids or Retinoids |
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