Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells.

Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Research Abstract Details 

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Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Abstract Text:

Shyam N Sundar,Vaishali Kerekatte,Caterina N Equinozio,Victor B Doan,Leonard F Bjeldanes,Gary L Firestone,

Estrogen-responsive breast cancer cells, such as MCF7 and T47D cells, express both estrogen receptor (ER)-alpha (ERalpha) and ERbeta. Indole-3-carbinol (I3C) strongly down-regulated ERalpha protein and transcript levels, without altering the level of ERbeta protein, in both cell lines. In cells transfected with the ERalpha promoter linked to a luciferase gene reporter, I3C ablated ERalpha promoter activity. Propyl pyrazole triol (PPT) is a highly selective ERalpha agonist, whereas, 17beta-estradiol activates both ERalpha and ERbeta. I3C treatment inhibited the PPT- and 17beta-estradiol-induced proliferation of breast cancer cells, disrupted the PPT and 17beta-estradiol stimulation of estrogen response element (ERE)-driven reporter plasmid activity as well as of endogenous progesterone receptor transcripts. Using an in vitro ERE binding assay, I3C was shown to inhibit the level of functional ERalpha and stimulated the level of ERE binding ERbeta even though the protein levels of this receptor remained constant. In ERalpha-/ERbeta+ MDA-MB-231 breast cancer cells, I3C treatment stimulated a 6-fold increase in binding of ERbeta to the ERE. I3C also induced ERE- and activator protein 1-driven reporter plasmid activities in the absence of an ER agonist, suggesting that ERbeta is activated in indole-treated cells. Taken together, our results demonstrate that the expression and function of ERalpha and ERbeta can be uncoupled by I3C with a key cellular consequence being a significantly higher ERbeta:ERalpha ratio that is generally highly associated with antiproliferative status of human breast cancer cells.

Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Publishing Authors By Initials

SN Sundar,V Kerekatte,CN Equinozio,VB Doan,LF Bjeldanes,GL Firestone,

For similar cells: cells, cultured: tumor cells, cultured research abstracts see: cells: cells, cultured: tumor cells, cultured research

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Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Molecular endocrinology (Baltimore, Md.)

VOLUME: 20

Page Numbers: 3070-82

Journal Abbreviation: Mol. Endocrinol.

ISSN: 0888-8809

DAY: 10

MONTH: 08

YEAR: 2006

Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8801431

Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Keywords Mesh Terms:

KEYWORDS: Tumor Cells, Cultured

MESH TERMS: drug effects

Chemical & Substance for Abstract: Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells. Information

Substance Name: indole-3-carbinol

Registry Number: 700-06-1

Grant and Affiliation Information for Indole-3-carbinol selectively uncouples expression and activity of estrogen receptor subtypes in human breast cancer cells.

AFFILIATION: Department of Molecular and Cell Biology, 591 LSA, University of California at Berkeley, Berkeley, California 94720-3200 USA.

Country: United States

AGENCY: United States NCI

GRANT: CA102360

ACRONYM: CA

MEDLINETA: Mol Endocrinol

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