6 Anticancer Effects of Indole-3-Carbinol and Its Dimer 3,3'-Diindolylmethane On Human Melanoma and Lung Cancer Cell Lines

Wednesday, November 4, 2009
Ballroom A+B (Camino Real Hotel)
Kristina Y. Aguilera , Biological Sciences, University of Texas at El Paso, El Paso, TX
Ida Aronchik, Dr. , Department of Molecular Cell Biology, University of California at Berkeley, Berkeley, CA
Kevin Poindexter , Department of Molecular Cell Biology, University of California at Berkeley, Berkeley, CA
Gary Firestone, Dr. , Department of Molecular Cell Biology, University of California at Berkeley, Berkeley, CA
Indole-3-carbinol (I3C) is an antiproliferative phytochemical produced from its precursor glucobrassicin in vegetables of the genus Brassica. I3C has been widely shown to suppress the proliferation of various human cancers including breast and prostate cells. Here, we investigate the anti-proliferative effects of I3C on malignant melanoma cells (G361), as well as the effects of I3C and DIM on the growth of human lung cancer cells (A549). We examined the effect of I3C and acetylsalicylic acid (ASA or aspirin) alone and in combination at various doses on G361 cell cycle progression, and activation of protein levels of key regulatory molecules involved in the control of cell growth. Our findings revealed that I3C together with aspirin synergistically induced cell cycle arrest in G1 phase, whereas treatment with I3C or aspirin, alone, had less effect on cell viability. This effect was associated with increase in p38/MAPK phosphorylation, while the total protein levels remained constant. We also observed increased levels in activating phosphorylation of p38/MAPK downstream target hsp27, which is frequently associated with the reduction of cell mobility in growth-arrested cells. A second focus of this investigation is to assess whether the I3C or its natural dimer 3,3’-Diindolylmethane (DIM) produce anti-proliferative effects in A549 lung cancer cells. Preliminary results demonstrate that all chosen doses of I3C show no significant difference in cell viability, while the experiments using DIM demonstrate a dose-dependent G1 cell cycle arrest. This study provides evidence of selective susceptibility of the A549 and G361 cell lines to I3C and DIM treatment.
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