J Cell Physiol. 2005 Jan 25; [Epub ahead of print] Links

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

Kang JS, Cho D, Kim YI, Hahm E, Kim YS, Jin SN, Kim HN, Kim D, Hur D,
Park H, Hwang YI, Lee WJ.

Department of Anatomy and Tumor Immunity Medical Research Center, Seoul
National University College of Medicine, Seoul, Korea.

Sodium ascorbate (vitamin C) has a reputation for inconsistent effects
upon malignant tumor cells, which vary from growth stimulation to
apoptosis induction. Melanoma cells were found to be more susceptible
to vitamin C toxicity than any other tumor cells. The present study has
shown that sodium ascorbate decreases cellular iron uptake by melanoma
cells in a dose- and time-dependent fashion, indicating that
intracellular iron levels may be a critical factor in sodium
ascorbate-induced apoptosis. Indeed, sodium ascorbate-induced apoptosis
is enhanced by the iron chelator, desferrioxamine (DFO) while it is
inhibited by the iron donor, ferric ammonium citrate (FAC). Moreover,
the inhibitory effects of sodium ascorbate on intracellular iron levels
are blocked by addition of transferrin, suggesting that transferrin
receptor (TfR) dependent pathway of iron uptake may be regulated by
sodium ascorbate. 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 demonstrates the specific mechanism of sodium
ascorbate-induced apoptosis and these findings support future clinical
trial of sodium ascorbate in the prevention of human melanoma relapse.
(c) 2005 Wiley-Liss, Inc.

PMID: 15672419 [PubMed - as supplied by publisher]

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