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Indole-3-carbinol enhances ultraviolet B-induced apoptosis by sensitizing human melanoma cells
Cited 41 time in
Web of Science
Cited 42 time in Scopus
- Authors
- Issue Date
- 2006-11-07
- Publisher
- Springer Verlag
- Citation
- Cell Mol Life Sci. 2006 Nov;63(22):2661-8.
- Keywords
- 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 ; bcl-2-Associated X Protein/metabolism ; Ultraviolet Rays
- Abstract
- 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.
- ISSN
- 1420-682X (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17086378
https://hdl.handle.net/10371/39188
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