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New research from the University of California in San Diego demonstrates instances in which the tumor suppressor protein p53 can boost cancer metabolism. The widely accepted idea is that p53 suppresses cancer but in some cancers it would have the opposite effect by promoting cancer. The protein p53 helps regulate growth and proliferation of cells. It responds to cellular stress, such as that which results from DNA damage, by halting the cell cycle or inducing apoptosis, a form of cell death.
In this way, p53 can help prevent rogue cells from forming malignant tumors. It is part of the body’s natural defense against cancer. Conversely, mutations of p53 that disrupt this function can contribute to cancer. Scientists have found, for example, that the gene that codes for p53 is one of the “most frequently mutated” in human cancers, and that the p53 pathway is inactive in most human cancers.
Cells get most of their energy from internal compartments called mitochondria, which produce fuel for metabolism in the form of ATP molecules.
Mitochondria typically use a process called oxidative phosphorylation to make ATP. However, in cancer cells, mitochondria favor a less efficient process called glycolysis, and they carry out less oxidative phosphorylation.
This switch to glycolysis involves p53 and another protein called p53 upregulated modulator of apoptosis (PUMA), which typically works with p53 to send damaged cells to programmed cell death. However, under certain conditions, it seems that PUMA can also trigger mitochondria to switch from oxidative phosphorylation to glycolysis, which favors cancer metabolism. Prof. Xu points out that at first, by lessening oxidative phosphorylation that generates “genome toxins,” p53 does prevent tumors. Once tumor growth is under way, however, p53 can work to support it. The findings should serve as a warning to cancer drug developers. Drugs that seek to fight cancer by restoring or enhancing the function of wild-type p53 could bring about the opposite result in some cancers.