ID2-ETS2 axis regulates the transcriptional acquisition of pro-tumoral microglia phenotype in glioma.


Journal

Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092

Informations de publication

Date de publication:
18 Jul 2024
Historique:
received: 18 02 2024
accepted: 09 07 2024
revised: 04 07 2024
medline: 18 7 2024
pubmed: 18 7 2024
entrez: 17 7 2024
Statut: epublish

Résumé

Glioblastoma is a highly aggressive brain tumour that creates an immunosuppressive microenvironment. Microglia, the brain's resident immune cells, play a crucial role in this environment. Glioblastoma cells can reprogramme microglia to create a supportive niche that promotes tumour growth. However, the mechanisms controlling the acquisition of a transcriptome associated with a tumour-supportive microglial reactive state are not fully understood. In this study, we investigated changes in the transcriptional profile of BV2 microglia exposed to C6 glioma cells. RNA-sequencing analysis revealed a significant upregulation of microglial inhibitor of DNA binding 1 (Id1) and Id2, helix-loop-helix negative transcription regulatory factors. The concomitant regulation of microglial ETS proto-oncogene 2, transcription factor (ETS2)-target genes, i.e., Dusp6, Fli1, Jun, Hmox1, and Stab1, led us to hypothesize that ETS2 could be regulated by ID proteins. In fact, ID2-ETS2 protein interactions increased in microglia exposed to glioma cells. In addition, perturbation of the ID2-ETS2 transcriptional axis influenced the acquisition of a microglial tumour-supportive phenotype. ID2 and ETS2 genes were found to be expressed by the tumour-associated microglia isolated from human glioblastoma tumour biopsies. Furthermore, ID2 and ETS2 gene expressions exhibited inverse prognostic values in patients with glioma in cohorts from The Cancer Genome Atlas. Collectively, our findings indicate that the regulation of ETS2 by ID2 plays a role in the transcriptional regulation of microglia in response to stimuli originating from glioblastoma cells, information that could lead to developing therapeutic strategies to manipulate microglial tumour-trophic functions.

Identifiants

pubmed: 39019900
doi: 10.1038/s41419-024-06903-3
pii: 10.1038/s41419-024-06903-3
doi:

Substances chimiques

Inhibitor of Differentiation Protein 2 0
Proto-Oncogene Protein c-ets-2 0
Proto-Oncogene Mas 0
MAS1 protein, human 0
ID2 protein, human 0
ETS2 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

512

Informations de copyright

© 2024. The Author(s).

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Auteurs

Guillermo Vázquez-Cabrera (G)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Martin Škandík (M)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Noémie Roncier (N)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Farah Real Oualit (F)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Mireia Cruz De Los Santos (M)

Department of Oncology Pathology, Karolinska Institutet, Stockholm, Sweden.

Austeja Baleviciute (A)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Mathilde Cheray (M)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Bertrand Joseph (B)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. bertrand.joseph@ki.se.
Center for Neuromusculoskeletal Restorative Medicine, Shui On Centre, Wan Chai, Hong Kong. bertrand.joseph@ki.se.

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