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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Sorted_tumor_DC RNAseq]

ABSTRACT: Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Sorted_tumor_DC RNAseq]

PROVIDER: PRJNA1175579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31058913_1.fastq.gz	Fastqsanger.gz
	SRR31058913_2.fastq.gz	Fastqsanger.gz
	SRR31058914_1.fastq.gz	Fastqsanger.gz
	SRR31058914_2.fastq.gz	Fastqsanger.gz
	SRR31058915_1.fastq.gz	Fastqsanger.gz

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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling

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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Synthesis [scRNAseq]

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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Bulk_Tumor_RNAseq]

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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Cell_Line_RNAseq]

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Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Cell_Line_RNAseq]

Project description:Therapeutic resistance to immune checkpoint blockade has been commonly linked to the process of mesenchymal transformation (MT) and remains a prevalent obstacle across many cancer types. An improved mechanistic understanding for MT-mediated immune evasion promises to lead to more effective combination therapeutic regimens. Herein, we identify the Hedgehog transcription factor, Gli2, as a key node of tumor-mediated immune evasion and immunotherapy resistance during MT. Mechanistic studies reveal that Gli2 generates an immunotolerant tumor microenvironment through the upregulation of Wnt ligand production and increased prostaglandin synthesis. This pathway drives the recruitment, viability, and function of granulocytic myeloid-derived suppressor cells (PMN-MDSCs) while also impairing type I conventional dendritic cell, CD8+ T cell, and NK cell functionality. Pharmacologic EP2/EP4 prostaglandin receptor inhibition and Wnt ligand inhibition each reverses a subset of these effects, while preventing primary and adaptive resistance to anti-PD-1 immunotherapy, respectively. A transcriptional Gli2 signature correlates with resistance to anti-PD-1 immunotherapy in stage IV melanoma patients, providing a translational roadmap to direct combination immunotherapeutics in the clinic.

2025-02-05 | GSE279935 | GEO

Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Bulk_Tumor_RNAseq]

2025-02-05 | GSE279934 | GEO

Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling

2025-02-05 | GSE280470 | GEO

Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Signaling [Sorted_tumor_DC RNAseq]

2025-02-05 | GSE279936 | GEO

Gli2 Facilitates Tumor Immune Evasion and Immunotherapeutic Resistance by Coordinating Wnt Ligand and Prostaglandin Synthesis [scRNAseq]

Project description:Therapeutic resistance to immune checkpoint blockade remains a prevalent obstacle across many cancer types, and an improved mechanistic understanding of this process could lead to effective combination treatments. Herein, we identify the Hedgehog transcription factor Gli2 as a key node of tumor-mediated immune evasion during mesenchymal transition via the production of Wnt ligands and prostaglandins. This promotes an immune microenvironment rich in PMN-MDSCs, while lacking antigen-presenting cDC1s and effector cells. Gli2-active tumors resist anti-PD-1 treatment, this can be overcome with inhibition of Wnt ligand secretion and selective prostaglandin receptor blockade. The identification of a Gli2 signature in patient samples provides a translational roadmap to direct precision combination immunotherapeutics in the clinic.

2025-02-05 | GSE279937 | GEO

Overexpression of GLI2 induces genomic instability

Project description:We used genome-wide microarray comparative genomic hybridization to investigate the response of control HT1080 cells and HT1080 cells infected with a lentivirus expressing eGFP, GLI2-eGFP or CCND1-RFP to challenge with methotrexate to address the question if GLI2 overexpression induces genomic instability. Keywords: aCGH Array CGH experiments of cell line genomic DNA as test samples and normal human genomic DNA as reference sample.

2009-01-05 | E-GEOD-10132 | biostudies-arrayexpress

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