Colorectal cancer cells with certain mutations "handle" vitamin C differently than other cells, and this difference ultimately kills them, finds a new study.
The idea that vitamin C could be an effective therapy for human cancer holds great appeal, but its track record in this arena has been more claim than data, with most clinical studies finding no evidence. Several ongoing clinical studies are exploring whether a therapeutic effect may require a high plasma level of vitamin C that can be achieved only by intravenous, not oral, administration.
In the meantime, the molecular mechanism by which vitamin C might selectively kill cancer cells remains unclear.
In a Science journal study, Jihye Yun and colleagues studied human colorectal cancer (CRC) cells with certain mutations in genes known as KRAS and BRAF, which regulate cell growth. They show that these cells take up the oxidized form of vitamin C through a certain receptor that is specifically over-expressed in the mutant cells.
This leads to oxidative stress, which in turn inactivates an enzyme required for growth of mutant but not normal cells. Consistent with the cell culture results, the authors found that administration of high-dose vitamin C to mice bearing intestinal tumors with the KRAS mutation inhibited tumor growth.
Moving forward, scientists can begin to explore whether the selective toxicity of vitamin C to these cells could be exploited to create vitamin C-based therapies.
