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Vitamin C as a Modulator of the Response to Cancer Therapy

1
Radiobiology Lab, The Greater Poland Cancer Centre, Garbary, 61-866 Poznan, Poland
2
Department of Head and Neck Surgery, Poznan University of Medical Sciences, The Greater Poland Cancer Centre, Garbary, 61-866 Poznan, Poland
3
Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, 60-355 Poznan, Poland
4
Centre for Orthodontic Mini-implants at the Department and Clinic of Maxillofacial Orthopedics and Orthodontics, Poznan University of Medical Sciences, 60-812 Poznan, Poland
5
Department of Pathology and Laboratory Medicine, Brown University, Providence, RI 02912, USA
*
Author to whom correspondence should be addressed.
Academic Editors: Simona Collina and Mariarosaria Miloso
Molecules 2019, 24(3), 453; https://doi.org/10.3390/molecules24030453
Received: 4 January 2019 / Revised: 24 January 2019 / Accepted: 26 January 2019 / Published: 28 January 2019
(This article belongs to the Special Issue Recent Advances in Anticancer Drugs)
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PDF [235 KB, uploaded 28 January 2019]

Abstract

Ascorbic acid (vitamin C) has been gaining attention as a potential treatment for human malignancies. Various experimental studies have shown the ability of pharmacological doses of vitamin C alone or in combinations with clinically used drugs to exert beneficial effects in various models of human cancers. Cytotoxicity of high doses of vitamin C in cancer cells appears to be related to excessive reactive oxygen species generation and the resulting suppression of the energy production via glycolysis. A hallmark of cancer cells is a strongly upregulated aerobic glycolysis, which elevates its relative importance as a source of ATP (Adenosine 5′-triphosphate). Aerobic glycolysis is maintained by a highly increased uptake of glucose, which is made possible by the upregulated expression of its transporters, such as GLUT-1, GLUT-3, and GLUT-4. These proteins can also transport the oxidized form of vitamin C, dehydroascorbate, permitting its preferential uptake by cancer cells with the subsequent depletion of critical cellular reducers as a result of ascorbate formation. Ascorbate also has a potential to affect other aspects of cancer cell metabolism due to its ability to promote reduction of iron(III) to iron(II) in numerous cellular metalloenzymes. Among iron-dependent dioxygenases, important targets for stimulation by vitamin C in cancer include prolyl hydroxylases targeting the hypoxia-inducible factors HIF-1/HIF-2 and histone and DNA demethylases. Altered metabolism of cancer cells by vitamin C can be beneficial by itself and promote activity of specific drugs. View Full-Text
Keywords: vitamin C; ascorbate; cancer; cancer therapy; chemotherapy; oxidative stress; ROS; hypoxia vitamin C; ascorbate; cancer; cancer therapy; chemotherapy; oxidative stress; ROS; hypoxia
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Blaszczak, W.; Barczak, W.; Masternak, J.; Kopczyński, P.; Zhitkovich, A.; Rubiś, B. Vitamin C as a Modulator of the Response to Cancer Therapy. Molecules 2019, 24, 453.

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