Genistein inhibits tamoxifen effects on cell proliferation and cell cycle arrest in T47D breast cancer cells

Julie L. Jones, Brian Daley, Blaine Enderson, Jin Rong Zhou, Michael Karlstad

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Tamoxifen is an antiestrogen used in the treatment of estrogen receptor-positive breast cancer in postmenopausal women. It functions by competitively inhibiting the estrogen receptor and inducing apoptosis and G 1 cell cycle arrest. Genistein is a soy phytoestrogen that inhibits breast cancer cell growth in vitro at doses of 10 μM or above. At lower doses genistein may stimulate cell growth and entry into the cell cycle. We hypothesized that treatment with low-dose genistein would reverse the inhibitory effects of tamoxifen in estrogen-receptor-positive breast cancer cells. Cell cycle kinetics and cell proliferation in T47-D human breast cancer cells were examined after exposure to genistein and tamoxifen in a low-estrogen environment designed to mimic a post-menopausal state. Cell proliferation was assessed by a colorimetric assay. Cell cycle kinetics were determined by flow cytometry. Tamoxifen caused G1 arrest and a decrease in proliferation. Genistein reversed the inhibitory effects of tamoxifen on both proliferation and G 1 arrest. Thus low-dose genistein was able to inhibit the therapeutic effects of tamoxifen in this postmenopausal model of breast cancer.

Original languageEnglish (US)
Pages (from-to)575-577
Number of pages3
JournalAmerican Surgeon
Volume68
Issue number6
StatePublished - Dec 1 2002

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Genistein
Tamoxifen
Cell Cycle Checkpoints
Cell Proliferation
Breast Neoplasms
Estrogen Receptors
Cell Cycle
Phytoestrogens
Gastrin-Secreting Cells
Estrogen Receptor Modulators
Therapeutic Uses
Growth
Flow Cytometry
Estrogens
Apoptosis
Therapeutics

All Science Journal Classification (ASJC) codes

  • Surgery

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Genistein inhibits tamoxifen effects on cell proliferation and cell cycle arrest in T47D breast cancer cells. / Jones, Julie L.; Daley, Brian; Enderson, Blaine; Zhou, Jin Rong; Karlstad, Michael.

In: American Surgeon, Vol. 68, No. 6, 01.12.2002, p. 575-577.

Research output: Contribution to journalArticle

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AB - Tamoxifen is an antiestrogen used in the treatment of estrogen receptor-positive breast cancer in postmenopausal women. It functions by competitively inhibiting the estrogen receptor and inducing apoptosis and G 1 cell cycle arrest. Genistein is a soy phytoestrogen that inhibits breast cancer cell growth in vitro at doses of 10 μM or above. At lower doses genistein may stimulate cell growth and entry into the cell cycle. We hypothesized that treatment with low-dose genistein would reverse the inhibitory effects of tamoxifen in estrogen-receptor-positive breast cancer cells. Cell cycle kinetics and cell proliferation in T47-D human breast cancer cells were examined after exposure to genistein and tamoxifen in a low-estrogen environment designed to mimic a post-menopausal state. Cell proliferation was assessed by a colorimetric assay. Cell cycle kinetics were determined by flow cytometry. Tamoxifen caused G1 arrest and a decrease in proliferation. Genistein reversed the inhibitory effects of tamoxifen on both proliferation and G 1 arrest. Thus low-dose genistein was able to inhibit the therapeutic effects of tamoxifen in this postmenopausal model of breast cancer.

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