L-Ascorbic acid (vitamin C) induces the apoptosis of B16 murine melanoma cells via a caspase-8-independent pathway
- Authors
- Kang, JS; Cho, DH; Kim, YI; Hahm, E; Yang, YH; Kim, D; Hur, D; Park, H; Bang, S; Hwang, YI; Lee, WJ
- Issue Date
- Nov-2003
- Publisher
- SPRINGER
- Keywords
- vitamin C; melanoma; apoptosis
- Citation
- CANCER IMMUNOLOGY IMMUNOTHERAPY, v.52, no.11, pp 693 - 698
- Pages
- 6
- Journal Title
- CANCER IMMUNOLOGY IMMUNOTHERAPY
- Volume
- 52
- Number
- 11
- Start Page
- 693
- End Page
- 698
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/16153
- DOI
- 10.1007/s00262-003-0407-6
- ISSN
- 0340-7004
1432-0851
- Abstract
- L-Ascorbic acid (vitamin C) has been reported to play a role in the treatment and prevention of cancer. However, its specific mechanistic pathways remain obscure. This study was carried out to identify the sodium ascorbate-induced apoptotic pathway in B16F10 murine melanoma cells. Sodium ascorbate was found to induce the apoptosis of B16F10 murine melanoma in a time- and dose-dependent manner, and this was prevented by pretreatment with N-acetyl-L-cysteine (NAC), a well-known antioxidant. In fact, sodium ascorbate-treated B16F10 melanoma cells showed increased intracellular reactive oxygen species generation (ROS) levels. These results indicate that sodium ascorbate induced apoptosis in B16F10 murine melanoma cells by acting as a prooxidant. We examined the involvement of caspase-8 using a specific caspase-8 inhibitor (z-IETD-fmk) on the sodium ascorbate-induced apoptotic pathway. Cell death was found not to be inhibited by z-IETD-fmk treatment, indicating that sodium ascorbate-induced apoptosis is not mediated by caspase-8. In addition, we detected a reduction in the mitochondrial membrane potential during apoptosis and confirmed cytochrome-c release from mitochondria by immunoblotting. Taken together, it appears that the induction of a prooxidant state by sodium ascorbate and a subsequent reduction in mitochondrial membrane potential are involved in the apoptotic pathway of B16F10 murine melanoma cells, and that this occurs in a caspase-8-independent manner.
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