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Targeting tumor-intrinsic N7-methylguanosine tRNA modification inhibits MDSC recruitment and improves anti-PD-1 efficacy

ABSTRACT: Targeting tumor-intrinsic N7-methylguanosine tRNA modification inhibits MDSC recruitment and improves anti-PD-1 efficacy

PROVIDER: PRJNA886424 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21782072.fastq.gz	Fastqsanger.gz
	SRR21782073.fastq.gz	Fastqsanger.gz
	SRR21782074.fastq.gz	Fastqsanger.gz
	SRR21782075.fastq.gz	Fastqsanger.gz
	SRR21782076.fastq.gz	Fastqsanger.gz

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Identification of potential readers for eukaryotic internal mRNA N7-methylguanosine (m7G) modification

Project description:The project aims to identify the RNA binding proteins that can specifically bind to mRNA internal modification N7-methylguanosine (m7G). N7-methylguanosine (m7G) methylation has been long identified as the essential cap modification for eukaryotic mRNA, but later has been identified internally in various types of RNAs, including tRNA, rRNA, miRNA, and mRNA. While the METTL1/WDR4 complex, responsible for tRNA m7G installation, has been suggested to be responsible for internal mRNA modification as well, little is known about the proteins that can identify and interact with m7G. To better understand its interaction with RNA binding proteins and further define its regulatory function in mRNA metabolism, we performed the experiment to pulldown proteins with different binding affinity on unmodified G and m7G and subject the enriched fractions to mass spectrometry.

2024-09-03 | PXD049390 | Pride

Transcriptome Mapping of Internal N7-methylguanosine modification via m7G MeRIP-seq [m7g.2]

Project description:Previous study found the presence of internal N7-methylguanosine (m7G) within mammalian mRNA. We performed antibody-based m7G MeRIP-seq for transcriptome-wide mapping the internal m7G sites in U2OS cells.

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Transcriptome Mapping of Internal N7-methylguanosine modification via m7G MeRIP-seq [m7g.1]

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Targeting tumor-intrinsic N7-methylguanosine tRNA modification inhibits MDSC recruitment and improves anti-PD-1 efficacy

Project description:We found that PMN-MDSCs level is elevated in the advanced ICCs tissues and is positively associated with the METTL1 and m7G tRNA modification levels. We further showed that impaired m7G tRNA modification impedes the PMN-MDSCs infiltration and inhibits ICC progression. Mechanistically, METTL1-mediated m7G tRNA modification selectively regulates the translation of human CXCL8 and mouse Cxcl5 transcripts, which facilitates the migration of PMN-MDSCs via binding to their cognate receptor CXCR2. Co-blockade of METTL1 and CXCR2 significantly enhances the efficacy of anti-PD-1 treatment in ICC. Taken together, our study reveals the cellular and molecular basis of crosstalk between ICC cells and MDSCs in shaping TIME and affecting ICIs efficacy, which enables reasonable design of new combined therapy targeting dysregulated mRNA translation and suppressive TIME.

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Pathogenic mechanism and therapeutic intervention of impaired N7-methylguanosine (m7G) tRNA modification [snRNA-seq]

Project description:The tRNA N7-methylguanosine (m7G) modification is not essential for yeast growth, but in mammals mis-regulations of tRNA m7G modification cause stem cell defect and developmental disorders. Here we found that homozygous mutated WDR4 caused microcephaly, retardation in motor coordination and spatial learning ability in mice, which mimics the symptom in human patients with WDR4 mutation. Further analysis revealed that homozygous mutation of WDR4 impaired tRNA m7G modification and reduced the translation level of genes involved in mTOR signaling pathway in mouse brain, which further caused endoplasmic reticulum (ER) stress and cell death. Our study uncovered a new layer of translation regulation mechanism mediated by tRNA m7G modification, provided strong evidence to support the important physiological function of mis-regulated tRNA modification in neuron disorders.

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Pathogenic mechanism and therapeutic intervention of impaired N7-methylguanosine (m7G) tRNA modification [TRAC-Seq]

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Pathogenic mechanism and therapeutic intervention of impaired N7-methylguanosine (m7G) tRNA modification [RNA-seq]

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Pathogenic mechanism and therapeutic intervention of impaired N7-methylguanosine (m7G) tRNA modification [RNC seq]

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N7-methylguanosine tRNA modification enhances oncogenic mRNA translation and promotes intrahepatic cholangiocarcinoma progression

Project description:The cancer cells selectively promote translation of specific oncogenic transcripts to facilitate cancer survival and progression, while the underlying mechanisms are poorly understood. N7-methylguanosine (m7G) tRNA modification and its methyltransferase complex METTL1/WDR4 are significantly up-regulated in intrahepatic cholangiocarcinoma (ICC) and associated with poor prognosis. We developed tRNA reduction and cleavage sequencing (TRAC-Seq) to reveal the m7G tRNA methylome inICC cell line and ribosome nascent-chain complex-bound mRNAs sequencing(RNC-seq) and ribosome profiling(Ribo-seq) to study the differential translated genes and reveal the ribosome pausing. A subset of 22 tRNAs is modified at a ‘RAGGU’ motif within the variable loop. We observe increased ribosome occupancy at the corresponding codons in the Mettl1 knockdown ICC cell line implying widespread effects on tRNA function, ribosome pausing, and mRNA translation. Translation of cell cycle genes and EGFR signaling pathway genes is particularly affected. Our study uncovers the important physiological function and mechanism of METTL1-mediated m7G tRNA modification in the regulation of cancer progression.

2021-08-07 | GSE161319 | GEO

N7-Methylguanosine tRNA modification promotes hepatocellular carcinoma metastasis after insufficient radiofrequency ablation

Project description:Radiofrequency heat ablation is an ideal radical cure for HCC treatment; however, insufficient radiofrequency ablation (IRFA) could lead to a high recurrence rate. N7-methylguanosine (m7G) on tRNAs is a heat-responding modification that is critical for yeast survival under high temperature, while its function and mechanism in HCC recurrence after IRFA are unknown. Here, we found that IRFA significantly up-regulates the level of m7G tRNA modification and its methyltransferase complex components METTL1 and WDR4 in multiple systems including HCC patient-derived xenograft (PDX) mouse, HCC tissues of patients, sublethal-heat-treated models of HCC cell lines and organoids. Functionally, gain- or loss-of function assays showed that METTL1 mediated m7G tRNA modification promotes HCC metastasis under sublethal heat exposure both in vitro and in vivo. Mechanistically, we found that METTL1 and m7G tRNA modification enhance the translation of SLUG and SNAIL in a codon frequency dependent manner under sublethal heat exposure. Overexpression of SLUG and SNAIL rescued the malignant potency of METTL1 knockdown HCC cells after sublethal heat stress. Our study uncovers the important physiological functions of m7G tRNA modification in heat stress responses and HCC recurrence after IRFA and suggests that targeting METTL1-m7G-SLUG and SNAIL axis could be a promising strategy to prevent HCC metastasis after radiofrequency heat ablation treatment.

2022-11-20 | GSE199966 | GEO

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