ArticleMolecular cancer therapeutics2008
Induction of growth arrest and apoptosis in human breast cancer cells by 3,3-diindolylmethane is associated with induction and nuclear localization of p27kip.
Article in Molecular cancer therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- 3,3'-Diindolylmethane Encapsulated Chitosan Nanoparticles Accelerates Inflammatory Markers, ER/PR, Glycoprotein and Mast Cells Population During Chemical Carcinogen Induced Mammary Cancer in Rats.Indian journal of clinical biochemistry : IJCB · 2018Article
- Chemopreventive properties of 3,3'-diindolylmethane in breast cancer: evidence from experimental and human studies.Nutrition reviews · 2016Review
- 3,39-Diindolylmethane Ameliorates Staphylococcal Enterotoxin B–Induced Acute Lung Injury through Alterations in the Expression of MicroRNA that Target Apoptosis and Cell-Cycle Arrest in Activated T Cells.The Journal of pharmacology and experimental therapeutics · 2016Article
- Multiple therapeutic and preventive effects of 3,3'-diindolylmethane on cancers including prostate cancer and high grade prostatic intraepithelial neoplasia.Journal of biomedical research · 2014Article
- Microwave-assisted, one-pot reaction of 7-azaindoles and aldehydes: a facile route to novel di-7-azaindolylmethanes.Tetrahedron letters · 2014Article
- 3,3'-diindolylmethane rapidly and selectively inhibits hepatocyte growth factor/c-Met signaling in breast cancer cells.The Journal of nutritional biochemistry · 2013Article
- Targeted regulation of PI3K/Akt/mTOR/NF-κB signaling by indole compounds and their derivatives: mechanistic details and biological implications for cancer therapy.Anti-cancer agents in medicinal chemistry · 2013Review
- Chemoprevention of lung tumorigenesis by intranasally administered diindolylmethane in A/J mice.Carcinogenesis · 2013Article
- RETRACTED: 3, 3'-Diindolylmethane enhances the effectiveness of herceptin against HER-2/neu-expressing breast cancer cells.PloS one · 2013Article
- 2,2'-diphenyl-3,3'-diindolylmethane: a potent compound induces apoptosis in breast cancer cells by inhibiting EGFR pathway.PloS one · 2013Article
- RETRACTED: Mechanisms and therapeutic implications of cell death induction by indole compounds.Cancers · 2011Article
- Urokinase plasminogen activator receptor and/or matrix metalloproteinase-9 inhibition induces apoptosis signaling through lipid rafts in glioblastoma xenograft cells.Molecular cancer therapeutics · 2010Article
- 3,3'-Diindolylmethane (DIM) inhibits the growth and invasion of drug-resistant human cancer cells expressing EGFR mutants.Cancer letters · 2010Article
- Down-regulation of uPA and uPAR by 3,3'-diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells.Journal of cellular biochemistry · 2009Article
- Endogenous HIV-1 Vpr-mediated apoptosis and proteome alteration of human T-cell leukemia virus-1 transformed C8166 cells.Apoptosis : an international journal on programmed cell death · 2009Article
- Effect of p27mt gene on apoptosis of the colorectal cancer cell line Lovo.World journal of gastroenterology · 2009Article
- Attenuation of multi-targeted proliferation-linked signaling by 3,3'-diindolylmethane (DIM): from bench to clinic.Mutation researchReview
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5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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 micromol/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.
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