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Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy

ABSTRACT: Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy

PROVIDER: PRJNA1094412 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28507128_1.fastq.gz	Fastqsanger.gz
	SRR28507128_2.fastq.gz	Fastqsanger.gz
	SRR28507129_1.fastq.gz	Fastqsanger.gz
	SRR28507129_2.fastq.gz	Fastqsanger.gz
	SRR28507130_1.fastq.gz	Fastqsanger.gz

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Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy

Project description:Despite notable advancements in cancer immunotherapy, the overall response rate among cancer patients remains low. Therefore, exploring strategies combining immunotherapy with adjuvant approaches to augment adaptive immune responses, such as by boosting the infiltration of T lymphocytes, is an attractive strategy. To pinpoint key regulators of tumor immunity, we developed a focused single guide RNA (sgRNA) library targeting membrane and secreted protein genes. Utilizing this library, we conducted an in vivo clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 screen in colorectal cancer mice model. We revealed that the loss of MBTPS1 in tumor cells enhanced anti-tumor immunity and synergized with anti-PD-1 therapy. Mechanistic studies uncovered that tumor cell-intrinsic MBTPS1 could compete with USP13 for binding with STAT1, thereby disrupting the USP13-dependent deubiquitination and stabilization of STAT1. MBTPS1 deficiency induced CXCR3+ CD8+ T cells infiltration in the tumor microenvironment by upregulating mRNA levels of Cxcl9, Cxcl10 and Cxcl11 transcribed by STAT1. Our study revealed that targeting MBTPS1 in cancer cells could turn cold tumors into inflamed ones, thereby enhancing the efficacy of anti-PD-1 blockade.

2025-03-14 | GSE262868 | GEO

Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy [scRNA-seq]

2025-03-14 | GSE263524 | GEO

Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy [scRNA-seq]

Project description:Inhibition of MBTPS1 reprograms cold into inflamed tumors and potentiates anti-PD-1 immunotherapy [scRNA-seq]

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Inhibition of Vps34 reprograms cold into hot inflamed tumors and improves anti-PD-1/PD-L1 immunotherapy.

Project description:One of the major challenges limiting the efficacy of anti-PD-1/PD-L1 therapy in nonresponding patients is the failure of T cells to penetrate the tumor microenvironment. We showed that genetic or pharmacological inhibition of Vps34 kinase activity using SB02024 or SAR405 (Vps34i) decreased the tumor growth and improved mice survival in multiple tumor models by inducing an infiltration of NK, CD8+, and CD4+ T effector cells in melanoma and CRC tumors. Such infiltration resulted in the establishment of a T cell-inflamed tumor microenvironment, characterized by the up-regulation of pro-inflammatory chemokines and cytokines, CCL5, CXCL10, and IFNγ. Vps34i treatment induced STAT1 and IRF7, involved in the up-regulation of CCL5 and CXCL10. Combining Vps34i improved the therapeutic benefit of anti-PD-L1/PD-1 in melanoma and CRC and prolonged mice survival. Our study revealed that targeting Vps34 turns cold into hot inflamed tumors, thus enhancing the efficacy of anti-PD-L1/PD-1 blockade.

| S-EPMC7190323 | biostudies-literature

Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

Project description:Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

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Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

Project description:Targeting METTL3 reprograms tumor microenvironment to improve cancer immunotherapy [RNA-seq]

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Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.

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Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

Project description:Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

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Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

Project description:Very low tumor mutation burden identifies inflamed recurrent glioblastomas responsive to cancer immunotherapy

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Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

Project description:Immune checkpoint blockade (ICB) has revolutionized cancer treatment, but the therapeutic response is highly heterogeneous. A potential mode of resistance is tumor-intrinsic mechanisms leading to an immunosuppressive tumor microenvironment. However, the underlying interactive network remains elusive and the generalizable biomarkers and targeting strategies are still lacking. Here, we uncovered the potential of plasma S100 calcium-binding protein A1 (S100A1) in determining ICB efficacy based on liquid biopsy of patients with lung cancer. Muti-omics and functional studies suggested that tumor-intrinsic S100A1 expression correlates with an immunologically cold TME and resistance to ICB. Mechanistic investigations demonstrated that interfering with tumor-intrinsic S100A1/ubiquitin-specific protease 7/p65/granulocyte-macrophage colony-stimulating factor (GM-CSF) modulatory axis could potentiate an inflamed TME via promoting M1-like macrophage polarization and T cell function. GM-CSF priming was sufficient to enhance ICB response in tumors with high S100A1 expression. These findings defined S100A1 as a potential biomarker and a novel synergistic target for cancer immunotherapy.

2025-03-26 | GSE285657 | GEO

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