Artigo Acesso aberto Revisado por pares

TIGAR, TIGAR, burning bright

2014; BioMed Central; Volume: 2; Issue: 1 Linguagem: Inglês

10.1186/2049-3002-2-1

ISSN

2049-3002

Autores

Pearl Lee, Karen H. Vousden, Eric C. Cheung,

Tópico(s)

Cancer Research and Treatments

Resumo

Cancers cells shift their metabolism towards glycolysis in order to help them support the biosynthetic demands necessary to sustain cell proliferation and growth, adapt to stress and avoid excessive reactive oxygen species (ROS) accumulation. While the p53 tumor suppressor protein is known to inhibit cell growth by inducing apoptosis, senescence and cell cycle arrest, recent studies have found that p53 is also able to influence cell metabolism. TIGAR is a p53 target that functions as a fructose-2,6-bisphosphatase, thereby lowering glycolytic flux and promoting antioxidant functions. By protecting cells from oxidative stress, TIGAR may mediate some of the tumor suppressor activity of p53 but could also contribute to tumorigenesis. Here we discuss the activities of TIGAR described so far, and the potential consequences of TIGAR expression on normal and tumor cells.

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