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Indole-3-carbinol enhances ultraviolet B-induced apoptosis by sensitizing human melanoma cells.
- Source :
-
Cellular and molecular life sciences : CMLS [Cell Mol Life Sci] 2006 Nov; Vol. 63 (22), pp. 2661-8. - Publication Year :
- 2006
-
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.
- Subjects :
- BH3 Interacting Domain Death Agonist Protein metabolism
Caspase 3 metabolism
Caspase 8 metabolism
Cell Line, Tumor
Cell Survival drug effects
Cell Survival radiation effects
Drug Synergism
Humans
Poly(ADP-ribose) Polymerases metabolism
Protein Transport drug effects
Proto-Oncogene Proteins c-bcl-2 metabolism
bcl-2-Associated X Protein metabolism
Apoptosis drug effects
Apoptosis radiation effects
Indoles pharmacology
Melanoma metabolism
Melanoma pathology
Ultraviolet Rays
Subjects
Details
- Language :
- English
- ISSN :
- 1420-682X
- Volume :
- 63
- Issue :
- 22
- Database :
- MEDLINE
- Journal :
- Cellular and molecular life sciences : CMLS
- Publication Type :
- Academic Journal
- Accession number :
- 17086378
- Full Text :
- https://doi.org/10.1007/s00018-006-6306-1