[en] BACKGROUND: Hypoxia is negatively associated with glioblastoma (GBM) patient survival and contributes to tumour resistance. Anti-angiogenic therapy in GBM further increases hypoxia and activates survival pathways. The aim of this study was to determine the role of hypoxia-induced autophagy in GBM. METHODS: Pharmacological inhibition of autophagy was applied in combination with bevacizumab in GBM patient-derived xenografts (PDXs). Sensitivity towards inhibitors was further tested in vitro under normoxia and hypoxia, followed by transcriptomic analysis. Genetic interference was done using ATG9A-depleted cells. RESULTS: We find that GBM cells activate autophagy as a survival mechanism to hypoxia, although basic autophagy appears active under normoxic conditions. Although single agent chloroquine treatment in vivo significantly increased survival of PDXs, the combination with bevacizumab resulted in a synergistic effect at low non-effective chloroquine dose. ATG9A was consistently induced by hypoxia, and silencing of ATG9A led to decreased proliferation in vitro and delayed tumour growth in vivo. Hypoxia-induced activation of autophagy was compromised upon ATG9A depletion. CONCLUSIONS: This work shows that inhibition of autophagy is a promising strategy against GBM and identifies ATG9 as a novel target in hypoxia-induced autophagy. Combination with hypoxia-inducing agents may provide benefit by allowing to decrease the effective dose of autophagy inhibitors.
Disciplines :
Oncologie
Auteur, co-auteur :
Abdul Rahim, Siti Aminah; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
Dirkse, Anne; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg. ; Faculty of Science, Technology and Communication, University of Luxembourg, Esch-sur-Alzette L-4365, Luxembourg.
Oudin, Anais; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
Schuster, Anne; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
BOHLER, Jill ; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
Barthelemy, Vanessa; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
Muller, Arnaud; Proteome and Genome Research Unit, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
Vallar, Laurent; Proteome and Genome Research Unit, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
JANJI, Bassam ; Laboratory of Experimental Cancer Research, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
GOLEBIEWSKA, Anna ; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg.
NICLOU, Simone P. ; NorLux Neuro-Oncology Laboratory, Department of Oncology, Luxembourg Institute of Health, L-1526 Luxembourg City, Luxembourg. ; KG Jebsen Brain Tumour Research Center, Department of Biomedicine, University of Bergen, N-5019 Bergen, Norway.
Co-auteurs externes :
yes
Langue du document :
Anglais
Titre :
Regulation of hypoxia-induced autophagy in glioblastoma involves ATG9A.
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