A low-dose arsenic-induced p53 protein-mediated metabolic mechanism of radiotherapy protection

Suthakar Ganapathy; Shaowen Xiao; Mei Yang; Min Qi; Doo Eun Choi; Chul S. Ha; John B. Little; Zhi Min Yuan

doi:10.1074/jbc.M113.531020

A low-dose arsenic-induced p53 protein-mediated metabolic mechanism of radiotherapy protection

Suthakar Ganapathy, Shaowen Xiao, Mei Yang, Min Qi, Doo Eun Choi, Chul S. Ha, John B. Little, Zhi Min Yuan

Department of Radiation Oncology

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

Abstract

Background: Radiotherapy protection depends on a selective protection of normal tissues but not tumors. Results: We demonstrate that low doses of arsenic induce a p53/HIF-1-dependent metabolic reprogramming specific to normal cells, resulting in increased resistance to radiation toxicity. Conclusion: p53-mediated metabolic reprogramming can be explored for normal tissue protection. Significance: The use of low-dose arsenic for selective protection of normal tissues may have important therapeutic implications.

Original language	English (US)
Pages (from-to)	5340-5347
Number of pages	8
Journal	Journal of Biological Chemistry
Volume	289
Issue number	8
DOIs	https://doi.org/10.1074/jbc.M113.531020
State	Published - Feb 21 2014

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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10.1074/jbc.M113.531020

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abstract = "Background: Radiotherapy protection depends on a selective protection of normal tissues but not tumors. Results: We demonstrate that low doses of arsenic induce a p53/HIF-1-dependent metabolic reprogramming specific to normal cells, resulting in increased resistance to radiation toxicity. Conclusion: p53-mediated metabolic reprogramming can be explored for normal tissue protection. Significance: The use of low-dose arsenic for selective protection of normal tissues may have important therapeutic implications.",

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AU - Qi, Min

AU - Choi, Doo Eun

AU - Ha, Chul S.

AU - Little, John B.

AU - Yuan, Zhi Min

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AB - Background: Radiotherapy protection depends on a selective protection of normal tissues but not tumors. Results: We demonstrate that low doses of arsenic induce a p53/HIF-1-dependent metabolic reprogramming specific to normal cells, resulting in increased resistance to radiation toxicity. Conclusion: p53-mediated metabolic reprogramming can be explored for normal tissue protection. Significance: The use of low-dose arsenic for selective protection of normal tissues may have important therapeutic implications.

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A low-dose arsenic-induced p53 protein-mediated metabolic mechanism of radiotherapy protection

Abstract

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