High-Dose Vitamin C Targets Redox Imbalance, Epigenetics, and Oxygen Sensing in Cancer
This review describes how pharmacological vitamin C exploits three shared cancer vulnerabilities: redox imbalance, epigenetic reprogramming via TET enzyme activation, and dysregulated oxygen sensing through HIF-1alpha. For clinical labs, the work highlights the need for validated biomarkers of oxidative stress and DNA hydroxymethylation status to identify patients most likely to benefit from high-dose vitamin C therapy.
The original study
Targeting cancer vulnerabilities with high-dose vitamin C.
- Authors
- Ngo B, Van Riper JM, Cantley LC, Yun J
- Journal
- Nature reviews. Cancer
- Type
- Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review
- PMID
- 30967651
Original abstract
Over the past century, the notion that vitamin C can be used to treat cancer has generated much controversy. However, new knowledge regarding the pharmacokinetic properties of vitamin C and recent high-profile preclinical studies have revived interest in the utilization of high-dose vitamin C for cancer treatment. Studies have shown that pharmacological vitamin C targets many of the mechanisms that cancer cells utilize for their survival and growth. In this Opinion article, we discuss how vitamin C can target three vulnerabilities many cancer cells share: redox imbalance, epigenetic reprogramming and oxygen-sensing regulation. Although the mechanisms and predictive biomarkers that we discuss need to be validated in well-controlled clinical trials, these new discoveries regarding the anticancer properties of vitamin C are promising to help identify patient populations that may benefit the most from high-dose vitamin C therapy, developing effective combination strategies and improving the overall design of future vitamin C clinical trials for various types of cancer.