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Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

ABSTRACT: Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

PROVIDER: PRJNA851367 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19763914_1.fastq.gz	Fastqsanger.gz
	SRR19763914_2.fastq.gz	Fastqsanger.gz
	SRR19763915_1.fastq.gz	Fastqsanger.gz
	SRR19763915_2.fastq.gz	Fastqsanger.gz
	SRR19763916_1.fastq.gz	Fastqsanger.gz

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Distinct cell adhesion signature defines glioblastoma myeloid-derived suppressor cell subsets

Project description:Increased myeloid-derived suppressor cell (MDSC) frequency is associated with worse outcomes and poor therapeutic response in multiple types of cancer. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared to granulocytic (g) MDSCs has yet to be determined. Here we performed first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in their behavior and found that mMDSCs and gMDSCs display differences in their tumor-accelerating ability, with mMDSCs driving tumor growth in GBM models. Epigenetic assessments revealed enhanced gene accessibility for cell adhesion programs in mMDSCs and higher integrin b1 expression and function in mouse and human mMDSCs. Integrin b1 blockage abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment. These findings suggest that integrin b1 expression underlies the enrichment of mMDSCs in tumors and represents a putative immunotherapy target to attenuate myeloid cell-driven immune suppression in GBM.

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Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets.

Project description:In multiple types of cancer, an increased frequency in myeloid-derived suppressor cells (MDSC) is associated with worse outcomes and poor therapeutic response. In the glioblastoma (GBM) microenvironment, monocytic (m) MDSCs represent the predominant subset. However, the molecular basis of mMDSC enrichment in the tumor microenvironment compared with granulocytic (g) MDSCs has yet to be determined. Here we performed the first broad epigenetic profiling of MDSC subsets to define underlying cell-intrinsic differences in behavior and found that enhanced gene accessibility of cell adhesion programs in mMDSCs is linked to their tumor-accelerating ability in GBM models upon adoptive transfer. Mouse and human mMDSCs expressed higher levels of integrin β1 and dipeptidyl peptidase-4 (DPP-4) compared with gMDSCs as part of an enhanced cell adhesion signature. Integrin β1 blockade abrogated the tumor-promoting phenotype of mMDSCs and altered the immune profile in the tumor microenvironment, whereas treatment with a DPP-4 inhibitor extended survival in preclinical GBM models. Targeting DPP-4 in mMDSCs reduced pERK signaling and their migration towards tumor cells. These findings uncover a fundamental difference in the molecular basis of MDSC subsets and suggest that integrin β1 and DPP-4 represent putative immunotherapy targets to attenuate myeloid cell-driven immune suppression in GBM.SignificanceEpigenetic profiling uncovers cell adhesion programming as a regulator of the tumor-promoting functions of monocytic myeloid-derived suppressor cells in glioblastoma, identifying therapeutic targets that modulate the immune response and suppress tumor growth.

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Myeloid-derived suppressor cell subsets drive glioblastoma growth in a sex-specific manner

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Coordinated chemokine expression defines macrophage subsets across tissues

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Coordinated chemokine expression defines macrophage subsets across tissues [scRNA-seq: mLu]

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Coordinated chemokine expression defines macrophage subsets across tissues [scRNA-seq: mSk]

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Coordinated chemokine expression defines macrophage subsets across tissues [scRNA-seq: mTumor]

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