The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Tp53-induced Glycolysis and Apoptosis Regulator (TIGAR) Protects Glioma Cells from Starvation-induced Cell Death by Up-regulating Respiration and Improving Cellular Redox Homeostasis
Open accessAbstract
Altered metabolism in tumor cells is increasingly recognized as a core component of the neoplastic phenotype. Because p53 has emerged as a master metabolic regulator, we hypothesized that the presence of wild-type p53 in glioblastoma cells could confer a selective advantage to these cells under the adverse conditions of the glioma microenvironment. Here, we report on the effects of the p53-dependent effector Tp53-induced glycolysis and apoptosis regulator (TIGAR) on hypoxia-induced cell death. We demonstrate that TIGAR is overexpressed in glioblastomas and that ectopic expression of TIGAR reduces cell death induced by glucose and oxygen restriction. Metabolic analyses revealed that TIGAR inhibits glycolysis and promotes respiration. Further, generation of reactive oxygen species (ROS) levels was reduced whereas levels of reduced glutathione were elevated in TIGAR-expressing cells. Finally, inhibiting the transketolase isoenzyme transketolase-like 1 (TKTL1) by siRNA reversed theses effects of TIGAR. These findings suggest that glioma cells benefit from TIGAR expression by (i) improving energy yield from glucose via increased respiration and (ii) enhancing defense mechanisms against ROS. Targeting metabolic regulators such as TIGAR may therefore be a valuable strategy to enhance glioma cell sensitivity toward spontaneously occurring or therapy-induced starvation conditions or ROS-inducing therapeutic approaches.
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Cites
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p53 Regulates Mitochondrial Respiration
Matoba, S., Kang, J.-G., Patino, W. D., Wragg, A., Boehm, M., Gavrilova, O., Hurley, P. J., Bunz, F., & Hwang, P. M. (2006) · Science · doi:10.1126/science.1126863 · Cited by 1,650
ROS-Generating Mitochondrial DNA Mutations Can Regulate Tumor Cell Metastasis
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Cited by
ROS and the DNA damage response in cancer
Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D. (2019) · Redox Biology · doi:10.1016/j.redox.2018.101084 · Cited by 2,144
The return of metabolism: biochemistry and physiology of the pentose phosphate pathway
Stincone, A., Prigione, A., Cramer, T., Wamelink, M. M. C., Campbell, K., Cheung, E., Olin‐Sandoval, V., Grüning, N., Krüger, A., Tauqeer Alam, M., et al. (2015) · Biological Reviews · doi:10.1111/brv.12140 · Cited by 1,576
ROS in Cancer: The Burning Question
Chio, I. I. C., & Tuveson, D. A. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.03.004 · Cited by 532
The enhancement of glycolysis regulates pancreatic cancer metastasis
Yang, J., Ren, B., Yang, G., Wang, H., Chen, G., You, L., Zhang, T., & Zhao, Y. (2020) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03278-z · Cited by 347
Mortenson, D. E., Brighty, G. J., Plate, L., Bare, G., Chen, W., Li, S., Wang, H., Cravatt, B. F., Forli, S., Powers, E. T., et al. (2018) · Journal of the American Chemical Society · doi:10.1021/jacs.7b08366 · Cited by 292
Metadata
- Authors
- Wanka, C., Steinbach, J. P., & Rieger, J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 287
- Issue
- 40
- Pages
- 33436-33446
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1984543978
- Cited by
- 162
- References
- 7
- FWCI
- 4.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Tp53-induced Glycolysis and Apoptosis Regulator (TIGAR) Protects Glioma Cells from Starvation-induced Cell Death by Up-regulating Respiration and Improving Cellular Redox Homeostasis. https://app.cochat.ai/papers/10.1074/jbc.m112.384578
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- Wanka, C., Steinbach, J. P., & Rieger, J. (2012). Tp53-induced Glycolysis and Apoptosis Regulator (TIGAR) Protects Glioma Cells from Starvation-induced Cell Death by Up-regulating Respiration and Improving Cellular Redox Homeostasis. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m112.384578
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