TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Karim Bensaad,Atsushi Tsuruta,Mary A. Selak,M. Nieves Calvo Vidal,Katsunori Nakano,Ramon Bartrons,Eyal Gottlieb,Karen H. Vousden +7 more
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TLDR
expression of TIGAR may modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired, and the decrease of intracellular ROS levels in response to TIGar may also play a role in the ability of p53 to protect from the accumulation of genomic damage.About:
This article is published in Cell.The article was published on 2006-07-14 and is currently open access. It has received 1803 citations till now. The article focuses on the topics: TP53-inducible glycolysis and apoptosis regulator & Apoptosis Regulator.read more
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Dealing with hunger: Metabolic stress responses in tumors
Michael A. Reid,Mei Kong +1 more
TL;DR: This review highlights recent studies that have brought insight into how cancer cells deal with low nutrient environments and elucidates the mechanisms used by cancer cells under nutrient restricted conditions.
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SP1 plays a pivotal role for basal activity of TIGAR promoter in liver cancer cell lines.
TL;DR: Data from electrophoretic mobility shift assay and chromatin immunoprecipitation showed that SP1 can interact with the SP1-binding site within TIGar promoter in vitro and in vivo, and concluded that SPl is indispensable for basal activity of TIGAR promoter.
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Metabolic pathways regulated by TAp73 in response to oxidative stress
TL;DR: The results suggest that in the absence of TAp73, H2O2 treatment results in an enhanced oxidative environment, and at the same time in an increased pro-anabolic phenotype, and indicates that TAp 73 exerts this function, at least partially, by regulation of cellular metabolism.
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Potential therapeutic targets of TP53 gene in the context of its classically canonical functions and its latest non-canonical functions in human cancer
TL;DR: The novel aspects of mutant p53 are summarized and its prominent therapeutic potentials in human cancer are described to suggest the activation of an oncogenic process through a gain of function (GOF).
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The decrease of glycolytic enzyme hexokinase 1 accelerates tumor malignancy via deregulating energy metabolism but sensitizes cancer cells to 2-deoxyglucose inhibition
Po Lin Tseng,Chih Wei Chen,Keng Hsun Hu,Hung Chi Cheng,Yuan Ho Lin,Wen Hui Tsai,Tain Junn Cheng,Wei Hsuan Wu,Chin Wei Yeh,Chin Chih Lin,Hui Ju Tsai,Hao-Chun Chang,Jiin Haur Chuang,Yan Shen Shan,Wen Tsan Chang +14 more
TL;DR: Results clearly indicate that the silencing of HK1, but not HK2, alters energy metabolism and induces an EMT phenotype, which enhances tumor malignancy, but increases the susceptibility of cancer cells to 2-DG inhibition, and suggests that the glycolytic inhibitors should be used only to treat cancers with elevated glyCOlytic activity.
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Surfing the p53 network
TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.
Lyubomir T. Vassilev,Binh Thanh Vu,Bradford Graves,Daisy Carvajal,Frank John Podlaski,Zoran Filipovic,Norman Kong,Ursula Kammlott,Christine Lukacs,Christian Klein,Nader Fotouhi,Liu Emily Aijun +11 more
TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
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Live or let die: the cell's response to p53
Karen H. Vousden,Xin Lu +1 more
TL;DR: Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.