TIGAR, TIGAR, burning bright.
TIGAR, TIGAR, burning bright.
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DOI：
10.1186/2049-3002-2-1
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发表时间：
2014-01-03
影响因子：
5.9
通讯作者：
Cheung EC
中科院分区：
文献类型：
--
作者：
Lee P;Vousden KH;Cheung EC
癌细胞将其代谢转向糖酵解，以帮助它们支持维持细胞增殖和生长、适应压力和避免过度活性氧（ROS）积累所必需的生物合成需求。虽然已知p53肿瘤抑制蛋白通过诱导细胞凋亡、衰老和细胞周期停滞来抑制细胞生长，但最近的研究发现p53还能够影响细胞代谢。TIGAR是p53的靶点，作为果糖-2,6-二磷酸酶，从而降低糖酵解通量并促进抗氧化功能。通过保护细胞免受氧化应激，TIGAR可能介导p53的一些肿瘤抑制活性，但也可能促进肿瘤发生。在这里，我们讨论到目前为止所描述的TIGAR的活性，以及TIGAR表达对正常细胞和肿瘤细胞的潜在影响。
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.