Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip.

Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Research Abstract Details 

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Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Abstract Text:

Zhiwei Wang,Bennett W Yu,Km Wahidur Rahman,Fakhara Ahmad,Fazlul H Sarkar,

3,3'-Diindolylmethane (DIM) is a stable condensation product of indole-3-carbanol, a potential breast cancer chemoprevention agent. Human breast cancer cell lines were studied to better understand its mechanisms. In vitro experiments were done in MCF-7, T47D, BT-20 and BT-474 cells using MTT, ELISA, immunoblotting assays, reverse transcription-PCR, protein half-life, confocal microscopy, cell fractionation, and immunoprecipitation assays. We found that DIM inhibited the growth of all four breast cancer cell lines (IC(50)s, 25-56 mumol/L). Because BT-20 and BT-474 overexpressed Her-2 and activated Akt, and BT-20 lacks estrogen receptor, these were studied further. In both cell lines, DIM appeared to induce expression of p27(kip) protein before the loss of cell viability and apoptosis. In BT-20 cells, DIM also inhibited expression of activated Akt, but this appeared after p27(kip) induction. In both cell lines, DIM induced p27(kip) transcript expression within 6 h. DIM prolonged the p27(kip) protein half-life in BT-20 but not BT-474 cells. We also showed, for the first time, that DIM induced nuclear localization of p27(kip) in both cell lines. Moreover, in BT-20 cells, DIM induced a decrease in p27(kip) phosphorylation at Thr(187), and its association with the 14-3-3 protein, which helped to explain the protein half-life increase and nuclear localization, respectively. DIM modulates p27(kip) through transcription, prolongation of protein half-life, and nuclear localization. These effects appear to be independent of Her-2, Akt, or estrogen receptor status and should support further study for its chemoprevention potential in breast cancer. [Mol Cancer Ther 2008;7(2):341-9].

Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Publishing Authors By Initials

Z Wang,BW Yu,KW Rahman,F Ahmad,FH Sarkar,

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Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Molecular cancer therapeutics

VOLUME: 7

Page Numbers: 341-9

Journal Abbreviation: Mol. Cancer Ther.

ISSN: 1535-7163

DAY: 18

MONTH: Feb

YEAR: 2008

Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip.

AFFILIATION: Department of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, 9374 Scott Hall, 540 East Canfield, Detroit, MI 48201. sarkarf@karmanos.org.

Country: United States

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