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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]

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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 MBTPS1 enhances antitumor immunity and potentiates anti-PD-1 immunotherapy

Project description:In this project, we transfected MC38 cells with Flag-tagged Mbtps1 or vector control. After that, we performed immunoprecipitation–mass spectrometry analysis to search the interacting proteins of MBTPS1. In our study, We observed that the loss of membrane-bound transcription factor site-1 protease (MBTPS1) in tumor cells enhanced antitumor immunity and potentiated anti-PD-1 therapy. Mechanistic studies revealed that tumor cell-intrinsic MBTPS1 competed with USP13 for binding to STAT1, thereby disrupting USP13-dependent deubiquitination and stabilization of STAT1. MBTPS1 deficiency induced CXCR3+ CD8+ T cell infiltration by upregulating STAT1-transcribed chemokines including CXCL9, CXCL10 and CXCL11. Notably, the regulatory role of MBTPS1 in antitumor immunity operates independently of its classic function in cleaving membrane-bound transcription factors. Collectively, our results provide a theoretical basis for MBTPS1 as a potential immunotherapy target and also as a predictor of immunotherapy efficacy.

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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.

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

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