GLS-driven glutamine catabolism contributes to prostate cancer radiosensitivity by regulating the redox state, stemness and ATG5-mediated autophagy
Anna Mukha(Helmholtz-Zentrum Dresden-Rossendorf), Uğur Kahya(Helmholtz-Zentrum Dresden-Rossendorf), Annett Linge(German Cancer Research Center), Oleg Chen(Helmholtz-Zentrum Dresden-Rossendorf), Steffen Löck(German Cancer Research Center), Vasyl Lukiyanchuk(Helmholtz-Zentrum Dresden-Rossendorf), Susan Richter(University Hospital Carl Gustav Carus), Tiago C. Alves(University Hospital Carl Gustav Carus), Mirko Peitzsch(University Hospital Carl Gustav Carus), Vladyslav Telychko(Helmholtz-Zentrum Dresden-Rossendorf), Sergej Skvortsov(Innsbruck Medical University), Giulia Negro(Innsbruck Medical University), Bertram Aschenbrenner(Innsbruck Medical University), Ira Skvortsova(Innsbruck Medical University), Peter Mirtschink(University Hospital Carl Gustav Carus), Fabian Lohaus(German Cancer Research Center), Tobias Hölscher(Helmholtz-Zentrum Dresden-Rossendorf), Hans Neubauer(Düsseldorf University Hospital), Mahdi Rivandi(Düsseldorf University Hospital), Vera Labitzky(Universität Hamburg), Tobias Lange(Universität Hamburg), André Franken(Düsseldorf University Hospital), Bianca Behrens(Düsseldorf University Hospital), Nikolas H. Stoecklein(Düsseldorf University Hospital), Marieta Toma(University of Bonn), Ulrich Sommer(University Hospital Carl Gustav Carus), Sebastian Zschaeck(German Cancer Research Center), Maximilian Rehm(German Cancer Research Center), Graeme Eisenhofer(University Hospital Carl Gustav Carus), Christian Schwager(German Cancer Research Center), Amir Abdollahi(German Cancer Research Center), Christer Groeben(University Hospital Carl Gustav Carus), Leoni A. Kunz‐Schughart(Helmholtz-Zentrum Dresden-Rossendorf), Gustavo Baretton(University Hospital Carl Gustav Carus), Michaël Baumann(German Cancer Research Center), Mechthild Krause(German Cancer Research Center), Claudia Peitzsch(German Cancer Research Center), Anna Dubrovska(German Cancer Research Center)
Cited by 168Open Access
Abstract
Radiotherapy is one of the curative treatment options for localized prostate cancer (PCa). The curative potential of radiotherapy is mediated by irradiation-induced oxidative stress and DNA damage in tumor cells. However, PCa radiocurability can be impeded by tumor resistance mechanisms and normal tissue toxicity. Metabolic reprogramming is one of the major hallmarks of tumor progression and therapy resistance. Specific metabolic features of PCa might serve as therapeutic targets for tumor radiosensitization and as biomarkers for
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