Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH
Abstract
Few experimental cancer therapies have incited as much debate as vitamin C. Yet the mechanistic effect of vitamin C on cancer cells is still poorly understood. Yun et al. studied human colorectal cancer cells with KRAS or BRAF mutations and found that they “handle” vitamin C in a different way than other cells, ultimately to their detriment (see the Perspective by Reczek and Chandel). Because a certain receptor is up-regulated in the mutant cells, they take up the oxidized form of vitamin C (dehydroascorbate). This leads to oxidative stress, inactivation of a glycolytic enzyme required by the mutant cells for growth, and finally cell death. Whether the selective toxicity of vitamin C to these mutant cells can be exploited therapeutically remains unclear.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Dec 11, 2015
- Source ID
- 10.1126/science.aaa5004
Entities
People
- Adam Kavalier
- Ashlesha Muley
- Carlo Rago
- Changyuan Lu
- Darryl J. Pappin
- Edouard Mullarky
- Eugenia G. Giannopoulou
- Iok In Christine Chio
- Jatin Roper
- Jihye Paik
- Jihye Yun
- John M Asara
- Kaitlyn N. Bosch
- Keith Rivera
- Lewis C. Cantley
- Lukas E Dow
- Nickolas Papadopoulos
- Olivier Elemento
- Steven S. Gross
- Zhengming Chen
Organizations
- Cold Spring Harbor Laboratory
- Damon Runyon Cancer Research Foundation
- Harvard Medical School
- National Cancer Institute
- National Institutes of Health
- Tufts Medical Center
- United States Department of Defense
- Weill Cornell Medicine