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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Sodium ascorbate inhibits growth via the induction of cell cycle arrest and apoptosis in human malignant melanoma A375.S2 cells
TLDR
Flow cytometric analysis showed that sodium ascorbate significantly induced cell cycle arrest and apoptosis in the A375.S2 cell line in a dose-dependent manner.
Ascorbate (vitamin C) induces cell death through the apoptosis-inducing factor in human breast cancer cells.
TLDR
It is demonstrated that ascorbate induces cell death through the apoptosis-inducing factor (AIF) in the human breast cancer cell lines, SK-BR3 and Hs578T, but not in a normal breast cell line, Hs580, and these results suggest that asCorbate activates a caspase-independent and AIF-mediated cell death pathway in human breast cancers.
Effects of transferrin receptor blockade on cancer cell proliferation and hypoxia-inducible factor function and their differential regulation by ascorbate.
TLDR
The addition of ascorbate increased the activity of the PHD enzymes in down-regulating HIF but not the proliferation of iron-starved anti-TfR mAb-treated cells, indicating that the use of anti- TfRmAbs and ascorBate in inhibiting both cell proliferation and HIF-1alpha and angiogenesis under normoxic conditions may be of therapeutic use.
Extracellular iron diminishes anticancer effects of vitamin C: An in vitro study
TLDR
It is shown, using two prostate cancer cell lines, that the anticancer/cytotoxic effects of ascorbate are completely abolished by iron at physiological concentrations in cell culture medium and human plasma.
Enhanced Anticancer Effect of Adding Magnesium to Vitamin C Therapy: Inhibition of Hormetic Response by SVCT-2 Activation
Combined arginine and ascorbic acid treatment induces apoptosis in the hepatoma cell line HA22T/VGH and changes in redox status involving the pentose phosphate pathway and reactive oxygen and nitrogen species.
High concentrations of ascorbic acid induces apoptosis of human gastric cancer cell by p38-MAP kinase-dependent up-regulation of transferrin receptor.
Ascorbate and Tumor Cell Iron Metabolism: The Evolving Story and its Link to Pathology.
TLDR
This paper demonstrates the anti-cancer activity of Asc through selective oxidative stress towards cancer cells via H2O2-generation at pharmacological concentrations and demonstrates that Asc's cytotoxic mechanism at concentrations (>1 mM) has been associated with decreased cellular iron uptake.
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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