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- W2912332372 abstract "4392 HT-29 and HCT-15 colon cancer cells express wild-type and mutant (K422Q) peroxisome proliferator-activated receptor (PPARγ) and rosiglitazone inhibits growth of HT-29 but not HCT-15 cells. This study investigates the mechanisms of HT-29 and HCT-15 cell growth inhibition by PPARγ active 1,1-bis (3’-indoyl)-1-(p-substituted phenyl methane) [C-substituted diindoyl methanes (DIMs)] that contain p-CF 3 (DIM-C-pPhCF 3 ), p-tbutyl (DIM-C-pPhtBu) and p-C 6 H 5 (DIM-C-pPhC 6 H 5 ) substituents. The PPARγ-active C-substituted DIMs inhibit greater than 50% of HT-29 and HCT-15 cell growth at concentrations of 1-5 and 5-10 μM respectively. Significant inhibition of G 0 /G 1 -S phase progression was observed in HT-29 but not in HCT-15 cells cultured in 2.5% charcoal-stripped serum. Inhibition of HT-29 and HCT-15 cell proliferation was not accompanied by significant changes in cyclin D1, p21 or p27 protein expression after treatment with 5.0 or 7.5 μM rosiglitazone, DIM-C-pPhCF 3 , DIM-C-pPhtBu or DIM-C-pPhC 6 H 5 . Protein levels of differentiation-inducible genes caveolin-1, caveolin-2 and keratin 18 were increased in HT-29 cells after treatment with rosiglitazone and the PPARγ-active C-substituted DIMs. In contrast, the C-substituted DIMs but not rosiglitazone induce caveolin-1 and caveolin-2 which may contribute to the differential ligand-dependent inhibition of HT-29 and HCT-15 cell growth." @default.
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- W2912332372 date "2004-04-01" @default.
- W2912332372 modified "2023-10-11" @default.
- W2912332372 title "Differential inhibition of HT-29 and HCT-15 colon cancer cell growth by rosiglitazone and 1,1-bis(3’-indolyl)-1-(p-substituted phenyl)methanes, a new class of peroxisome proliferator-activated receptor γ agonists" @default.
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