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Nat Commun ; 12(1): 6130, 2021 10 21.
Artigo em Inglês | MEDLINE | ID: mdl-34675201

RESUMO

Epigenetic mechanisms which play an essential role in normal developmental processes, such as self-renewal and fate specification of neural stem cells (NSC) are also responsible for some of the changes in the glioblastoma (GBM) genome. Here we develop a strategy to compare the epigenetic and transcriptional make-up of primary GBM cells (GIC) with patient-matched expanded potential stem cell (EPSC)-derived NSC (iNSC). Using a comparative analysis of the transcriptome of syngeneic GIC/iNSC pairs, we identify a glycosaminoglycan (GAG)-mediated mechanism of recruitment of regulatory T cells (Tregs) in GBM. Integrated analysis of the transcriptome and DNA methylome of GBM cells identifies druggable target genes and patient-specific prediction of drug response in primary GIC cultures, which is validated in 3D and in vivo models. Taken together, we provide a proof of principle that this experimental pipeline has the potential to identify patient-specific disease mechanisms and druggable targets in GBM.


Assuntos
Neoplasias Encefálicas/genética , Glioblastoma/genética , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neurais/metabolismo , Animais , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/fisiopatologia , Diferenciação Celular , Metilação de DNA , Epigênese Genética , Epigenômica , Glioblastoma/metabolismo , Glioblastoma/fisiopatologia , Humanos , Camundongos , Transcrição Gênica
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