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RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [Ribo-Seq]

ABSTRACT: RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [Ribo-Seq]

PROVIDER: PRJNA1144916 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30149182.fastq.gz	Fastqsanger.gz
	SRR30149183.fastq.gz	Fastqsanger.gz
	SRR30149184.fastq.gz	Fastqsanger.gz
	SRR30149185.fastq.gz	Fastqsanger.gz

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RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [Ribo-Seq]

Project description:The role of N1-methyladenosine (m1A) in cancer remains poorly understood. Here we investigate the functional importance of RNA m1A methyltransferase TRMT61A in colorectal cancer (CRC) and assess its potential as a therapeutic target. Our findings demonstrate consistent elevation of TRMT61A expression and RNA m1A levels in primary CRC tissues, which correlate significantly with poor patient survival. Through CRISPR/Cas9 screenings, TRMT61A is the most essential gene among m1A regulators. We further elucidate that TRMT61A facilitates CRC tumorigenesis and progression by enhancing the stability of mRNA of crucial targets, including ONECUT2, thereby activating the MAPK/ERK signaling pathway in an m1A-dependent manner. Of note, we show promising anti-CRC effects by inhibiting TRMT61A using nanoparticleencapsulated siTRMT61A or our identified small molecule compound, PGG. Collectively, our study uncovers the essential role of TRMT61A-m1A in CRC by activating the ONECUT2-MAPK/ERK pathway. Targeting TRMT61A holds promise as a therapeutic approach for treating CRC.

2025-02-01 | GSE274079 | GEO

RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer II

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RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer I

2025-02-01 | GSE274027 | GEO

RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [MeRIP-Seq]

2025-02-01 | GSE274076 | GEO

RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer II

Project description:RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer II

| PRJNA1144484 | ENA

RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer I

Project description:RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer I

| PRJNA1144485 | ENA

RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [MeRIP-Seq]

Project description:RNA m1A methyltransferase TRMT61A induces MAPK/ERK signaling and is a therapeutic target in colorectal cancer [MeRIP-Seq]

| PRJNA1144905 | ENA

tRNA m1A modification regulates cholesterol biosynthesis to promote antitumor immunity of CD8+ T cells

Project description:Activation of CD8+ T cells necessitates rapid metabolic reprogramming to fulfill the substantial biosynthetic demands of their effector functions. However, the post-transcriptional mechanisms underpinning this process remain obscure. The tRNA N1-methyladenine (m1A) modification, which plays a role in maintaining tRNA stability and modulating protein translation, has an undefined physiological function in CD8+ T cells, particularly in antitumor responses. Here, we demonstrate that the tRNA m1A 'writer' gene Trmt61a enhances the tumor-killing capacity of CD8+ T cells by regulating cholesterol biosynthesis. We find that Trmt61a expression in CD8+ T cells is upregulated upon activation and correlates positively with T cell-mediated cytotoxicity within the tumor microenvironment of colorectal cancer (CRC) patients. Deletion of Trmt61a in CD8+ T cells leads to a compromised tumor-killing function in both in vivo and in vitro assays, which is dependent on the m1A catalytic activity of TRMT61A. Mechanistically, tRNA m1A promotes antitumor immunity in CD8+ T cells by enhancing the translation of ATP citrate lyase (ACLY), a key enzyme for cholesterol biosynthesis. Supplementation with cholesterol can rescue the impaired tumor-killing function and proliferation of TRMT61A-deficient CD8+ T cells. Our findings underscore the significance of tRNA m1A modification as a regulatory checkpoint in cholesterol metabolism in CD8+ T cells, suggesting potential novel strategies for cancer immunotherapy.

2025-01-07 | GSE275602 | GEO

m1A inhibition fuels oncolytic virus-elicited antitumor immunity via downregulating PD-L1 expression

Project description:RNA N1-methyladenosine methylation (m1A) modification is critical in regulating mRNA translation and thus protein synthesis, but the role of m1A modification in the occurrence, progression, and immunotherapy of head and neck squamous cell cancer (HNSCC) remains largely unknown. In Tgfbr1/Pten 2cKO mice, we found that the spontaneous neoplastic transformation of oral mucosa is accompanied by elevated levels of m1A modification. Analysis of m1A-associated genes identified TRMT61A as the key m1A writer associated with cancer progression, and poor prognosis. Mechanically, TRMT61A-induced tRNA-m1A modification promotes MYC protein synthesis and subsequent programmed death-ligand 1 (PD-L1) expression. In Tgfbr1/Pten 2cKO mice, RNA-m1A modification levels are also elevated in tumors that developed resistance to oncolytic herpes simplex virus (oHSV) treatment. Therapeutic inhibition of m1A modification sustains oncolytic virus-induced antitumor immunity and reduces tumor growth, providing a promising strategy for alleviating resistance to oHSV therapy. These findings indicate that m1A inhibition can prevent immune escape after oHSV therapy by reducing the expression of PD-L1. Our results provide a mutually reinforcing strategy for clinical combination immunotherapy.

2024-03-31 | GSE247024 | GEO

Chemical manipulation of m1A mediates its detection in human tRNA

Project description:N1-methyl adenosine (m1A) is a wide-spread RNA modification present in tRNA, rRNA and mRNA. m1A modification sites in tRNAs are evolutionary conserved and its formation on tRNA is catalyzed by methyltransferase TRMT61A and TRMT6 complex. m1A promotes translation initiation and elongation. Due to its positive charge under physiological conditions, m1A can notably modulate RNA structure. It also blocks Watson-Crick base pairing and causes mutation and truncation during reverse transcription. Several misincorporation-based high throughput sequencing methods have been developed to sequence m1A. In this study, we introduce a reduction-based m1A sequencing (red-m1A-seq). We report that NaBH4 reduction of m1A can improve the mutation and readthrough rates using commercially available RT enzymes to give better positive signature, while alkaline-catalyzed Dimroth rearrangement can efficiently convert m1A to m6A to provide good controls, allowing the detection of m1A with higher sensitivity and accuracy. We applied red‑m1A-seq to sequence human small RNA and we not only detected all the previously reported tRNA m1A sites, but also new m1A sites in mt-tRNAAsn-ATT and 5.8S rRNA.

2024-04-24 | GSE253657 | GEO

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