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WT or Usp5 knockout (KO) PMs were infected with HSV-1 or not

ABSTRACT: WT or Usp5 knockout (KO) PMs were infected with HSV-1 or not

PROVIDER: PRJNA978004 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24774648_1.fastq.gz	Fastqsanger.gz
	SRR24774648_2.fastq.gz	Fastqsanger.gz
	SRR24774649_1.fastq.gz	Fastqsanger.gz
	SRR24774649_2.fastq.gz	Fastqsanger.gz
	SRR24774650_1.fastq.gz	Fastqsanger.gz

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WT or Usp5 knockout (KO) PMs were infected with HSV-1 or not

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PMs were infected with HSV-1 or not

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Transcription profiling by array to investigate USP5 knock out in cardiomycytes

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USP5 stabilizes YTHDF1 to control cancer immune surveillance through mTORC1-mediated phosphorylation

Project description:N6-methyladenosine (m6A) binding protein YTHDF1 is frequently upregulated in various cancers and its depletion enhances the efficacy of immune checkpoint blockade (ICB) therapy. This study reveals that USP5 interacts with YTHDF1, preventing its K11-linked polyubiquitination, thereby stabilizing YTHDF1 and promoting its oncogenic properties. In response to insulin, mTORC1 phosphorylates USP5, facilitating its dimerization and subsequent binding to YTHDF1, while the CUL7-FBXW8 complex promotes its degradation. Notably, YTHDF1 or USP5 deficiency increases PD-L1 expression and impairs immune response gene expression, contributing to immune evasion. Combining USP5 inhibitors with anti-PD-1 therapy enhances antitumor T-cell immunity and improves tumor regression in mouse models. Thus, USP5 may serve as a biomarker for stratifying patients for anti-PD-1 therapy, suggesting a novel strategy of combining USP5 inhibition with PD-(L)1 blockade to enhance cancer treatment efficacy.

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USP5 stabilizes YTHDF1 to control cancer immune surveillance through mTORC1-mediated phosphorylation

Project description:The N6-methyladenosine (m6A) binding protein YTHDF1 emerges as a frequently upregulated oncogene across various cancer types. Its depletion significantly improves the efficacy of cancer immune checkpoint blockade (ICB) treatment. A comprehensive understanding of the molecular mechanisms governing YTHDF1 protein stability is pivotal for enhancing clinical response rates and the effectiveness of ICB in cancer patients. Here, we report that USP5 interacts with YTHDF1, removing K11-linked polyubiquitination on multiple lysine residues to stabilize YTHDF1, thereby conferring its oncogenic properties. In response to insulin, mTORC1 phosphorylates USP5 at S149, promoting its dimerization. Dimerized USP5 then binds to YTHDF1, preventing its degradation. Conversely, the CUL7-FBXW8 E3 ubiquitin ligase promotes K11-linked polyubiquitination and degradation of YTHDF1. USP5 and FBXW8 thus regulate YTHDF1 ubiquitylation at defined residues through mutually exclusive interactions and opposing activities. Furthermore, deficiency in YTHDF1 or USP5 enhances PD-L1 expression and compromises the expression of multiple immune response-related genes, fostering cancer immune evasion. Remarkably, combining USP5 inhibitor treatment with anti-PD-1 immunotherapy reprograms the antitumor T-cell immunity environment, leading to enhanced tumor regression and markedly improved overall survival rates in mouse tumor models. Therefore, in hepatocellular carcinoma and lung cancer patients, USP5 may serve as a promising biomarker for stratifying individuals for anti-PD-1 therapy. Our findings reveal a ubiquitination-dependent regulation of YTHDF1 protein stability influencing immune response gene expression, suggesting USP5 inhibition combined with PD-(L)1 blockade as a novel and promising strategy for cancer treatment.

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