Autophagy inhibition sensitizes radiotherapy responses in high-grade mutant IDH1 glioma

Mutant isocitrate dehydrogenase 1 (mIDH1) catalyzes 2-hydroxyglutarate (2HG) production which leads to epigenetic reprogramming in astrocytomas with tumor protein p53 (TP53)/α-thalassemia/mental retardation, X-linked (ATRX) loss. RNA-sequencing, single-cell RNA-sequencing, and Chromatin Immunoprecipitation sequencing (ChIP-seq) followed by bioinformatics analysis shows that human and mouse mIDH1 gliomas exhibit downregulated gene ontologies (GOs) related to mitochondrial metabolism and upregulated autophagy-related GOs. Decreased mitochondrial metabolism is accompanied by decreased glycolysis, rendering autophagy as a source of energy in mIDH1 gliomas. Mutant IDH1 glioma cells exhibit increased expression of autophagy-related proteins and enhanced microtubule-associated protein 1 light chain 3 (LC3) I/II conversion, indicating augmented autophagy. Inhibiting autophagy in vivo by administration of synthetic protein nanoparticles (SPNPs) encapsulating autophagy related gene 7 (ATG7) silencing RNA sensitizes mIDH1 glioma cells to radiation, resulting in tumor regression, long-term survival, and immunological memory. This work uncovers autophagy as a critical pathway for survival in mIDH1 gliomas and its inhibition elicits radiosensitivity in vitro in human and mouse mIDH1 glioma cells, and in vivo in mIDH1 models.

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Publication Details

Journal
Nature Communications
Published
2026-09-18
DOI
https://doi.org/10.1038/s41467-026-77320-7
Primary Topic
Autophagy in Disease and Therapy
Type
article
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article

Autophagy inhibition sensitizes radiotherapy responses in high-grade mutant IDH1 glioma

Peter Sajjakulnukit, Stephen V. Carney, Ziwen Zhu, Andrea Comba et al.
Nature Communications
Autophagy in Disease and Therapy
article

Autophagy inhibition sensitizes radiotherapy responses in high-grade mutant IDH1 glioma

Peter Sajjakulnukit, Stephen V. Carney, Ziwen Zhu, Andrea Comba, Brandon L. McClellan, Jorge A. Peña Agudelo, Maureen A. Sartor, Joshua D. Welch, Julio Zelaya, Kaushik Banerjee, Shi‐Yuan Cheng, Zeribe C. Nwosu, Mats Ljungman, Mahmoud S. Alghamri, Joerg Lahann, Padma Kadiyala, Pedro R. Löwenstein, María G. Castro, Claire E. Tronrud, Adam Klaiss, Sadhakshi Raghuram, Tingting Qin, Ayman Taher, Maria B. Garcia-Fabiani, Maya R. Sheth, Hanna S. Hong, Costas A. Lyssiotis, Felipe J. Núñez, Anzar A. Mujeeb, Ava Mauser
article en

Abstract

Mutant isocitrate dehydrogenase 1 (mIDH1) catalyzes 2-hydroxyglutarate (2HG) production which leads to epigenetic reprogramming in astrocytomas with tumor protein p53 (TP53)/α-thalassemia/mental retardation, X-linked (ATRX) loss. RNA-sequencing, single-cell RNA-sequencing, and Chromatin Immunoprecipitation sequencing (ChIP-seq) followed by bioinformatics analysis shows that human and mouse mIDH1 gliomas exhibit downregulated gene ontologies (GOs) related to mitochondrial metabolism and upregulated autophagy-related GOs. Decreased mitochondrial metabolism is accompanied by decreased glycolysis, rendering autophagy as a source of energy in mIDH1 gliomas. Mutant IDH1 glioma cells exhibit increased expression of autophagy-related proteins and enhanced microtubule-associated protein 1 light chain 3 (LC3) I/II conversion, indicating augmented autophagy. Inhibiting autophagy in vivo by administration of synthetic protein nanoparticles (SPNPs) encapsulating autophagy related gene 7 (ATG7) silencing RNA sensitizes mIDH1 glioma cells to radiation, resulting in tumor regression, long-term survival, and immunological memory. This work uncovers autophagy as a critical pathway for survival in mIDH1 gliomas and its inhibition elicits radiosensitivity in vitro in human and mouse mIDH1 glioma cells, and in vivo in mIDH1 models.

Nature CommunicationsVol. 17(1)
Northwestern University (US), University of Michigan (US), Michigan Medicine (US), Michigan Center for Translational Pathology (US), Robert H. Lurie Comprehensive Cancer Center of Northwestern University
Openalex Percentile: Top 11%
Autophagy in Disease and Therapy
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