S-Space College of Medicine/School of Medicine (의과대학/대학원) Molecular and Genomic Medicine (분자유전체의학전공) Journal Papers (저널논문_분자유전체의학전공)
Indole-3-carbinol enhances ultraviolet B-induced apoptosis by sensitizing human melanoma cells
- Kim, D-S; Jeong, Y-M; Moon, S-I; Kim, S-Y; Kwon, S-B; Park, E-S; Youn, S-W; Park, K-C
- Issue Date
- Springer Verlag
- Cell Mol Life Sci. 2006 Nov;63(22):2661-8.
- Apoptosis/*drug effects/*radiation effects; BH3 Interacting Domain Death Agonist Protein/metabolism; Caspase 3/metabolism; Caspase 8/metabolism; Cell Line, Tumor; Cell Survival/drug effects/radiation effects; Drug Synergism; Humans; Indoles/*pharmacology; Melanoma/*metabolism/*pathology; Poly(ADP-ribose) Polymerases/metabolism; Protein Transport/drug effects; Proto-Oncogene Proteins c-bcl-2/metabolism; *Ultraviolet Rays; bcl-2-Associated X Protein/metabolism
- Indole-3-carbinol (I3C) has been found to act against several types of cancer, while ultraviolet B (UVB) is known to induce the apoptosis of human melanoma cells. Here, we investigated whether I3C can sensitize G361 human melanoma cells to UVB-induced apoptosis. We examined the effects of combined I3C and UVB (I3C/UVB) at various dosages. I3C (200 microM)/UVB (50 mJ/cm(2)) synergistically reduced melanoma cell viability, whereas I3C (200 microM) or UVB (50 mJ/cm(2)), separately, had little effect on cell viability. DNA fragmentation assays indicated that I3C/UVB induced apoptosis. Further results show that I3C/UVB activates caspase-8, -3, and Bid and causes the cleavage of poly(ADP-ribose) polymerase. Moreover, I3C decreased the expression of the anti-apoptotic protein, Bcl-2, whereas UVB increased the translocation of Bax to mitochondria. Thus, an increased Bax/Bcl-2 ratio by I3C/UVB may result in melanoma apoptosis. In conclusion, our study demonstrated that I3C sensitizes human melanoma cells by down-regulating Bcl-2.
- 1420-682X (Print)
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