Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down‐regulation of transferrin receptor dependent iron uptake

@article{Kang2005SodiumA,
  title={Sodium ascorbate (vitamin C) induces apoptosis in melanoma cells via the down‐regulation of transferrin receptor dependent iron uptake},
  author={Jae Seung Kang and Daeho Cho and Young-In Kim and Eunsil Hahm and YeongSeok Kim and Shun Nu Jin and Ha Na Kim and Daejin Kim and Dae Young Hur and Hyunjeong Park and Young-Il Hwang and Wang Jae Lee},
  journal={Journal of Cellular Physiology},
  year={2005},
  volume={204}
}
Sodium ascorbate (vitamin C) has a reputation for inconsistent effects upon malignant tumor cells, which vary from growth stimulation to apoptosis induction. [] Key Result Cells exposed to sodium ascorbate demonstrated down-regulation of TfR expression and this precedes sodium ascorbate-induced apoptosis. Taken together, sodium ascorbate-mediated apoptosis appears to be initiated by a reduction of TfR expression, resulting in a down-regulation of iron uptake followed by an induction of apoptosis. This study…
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TLDR
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TLDR
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Ascorbate and Tumor Cell Iron Metabolism: The Evolving Story and its Link to Pathology.
TLDR
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Vitamin C down‐regulates VEGF production in B16F10 murine melanoma cells via the suppression of p42/44 MAPK activation
TLDR
The data suggest that vitamin C can down‐regulate VEGF production via the modulation of COX‐2 expression and that p42/44 MAPK acts as an important signaling mediator in this process.
SVCT-2 in breast cancer acts as an indicator for L-ascorbate treatment
TLDR
It is demonstrated that L-ascorbate has a selective killing effect, which is influenced by sodium-dependent vitamin C transporter 2 (SVCT-2) in human breast cancer cells, and functional SVCT- 2 sensitizes breast cancer Cells to autophagic damage by increasing the L-ASCorbate concentration and intracellular ROS production.
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