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Dietary glucose affects the levels of a powerful oncogene in mice
Date:11/14/2012

ncer cells, engrafted in mice, to grow when the animals were fed one of two diets low or high carbohydrates. In this case the researchers constructed a p53 mutant protein that was less susceptible to degradation by glucose restriction-induced autophagy.

They found that in the mice fed the low carbohydrate diet, the growth of tumors was blocked, but only when the tumors expressed the mutant p53 protein that could be degraded by autophagy. But when the artificial mutant p53 proteins could not be cleared, cancer growth proceeded regardless of the glucose content in the diet. This suggested that p53 mutant degradation is part of the reason why the low carbohydrate diet slows tumor growth, Avantaggiati says.

"This series of studies helps establish the mechanisms of why a low carbohydrate diet slows tumor growth," says Avantaggiati. "Glucose restriction triggers autophagy, a critical process for clearing the cell of detrimental, potentially damaging proteins or cellular debris that can eventually destroy the entire cancer cell. We believe that this process works more efficiently when mutant p53 is not around."

The findings are very compelling, she says, and should set the ground for investigating, in further depth, how glucose and various food components affect the levels of mutant p53 in tumors. "Various types of dietetic interventions have been shown to affect cancer growth, but no one had ever shown, before this study, that the amount of carbohydrates could affect the expression of mutant p53," Avantaggiati says. "However, we need to be cautious about translating a finding from mice to humans. Our research into that connection is ongoing."


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Contact: Karen Mallet
km463@georgetown.edu
Georgetown University Medical Center
Source:Eurekalert

Page: 1 2 3

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