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

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

PROVIDER: PRJNA1144484 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30159712_1.fastq.gz	Fastqsanger.gz
	SRR30159712_2.fastq.gz	Fastqsanger.gz
	SRR30159713_1.fastq.gz	Fastqsanger.gz
	SRR30159713_2.fastq.gz	Fastqsanger.gz
	SRR30159714_1.fastq.gz	Fastqsanger.gz

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

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 | GSE274027 | GEO

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

2025-02-01 | GSE274028 | 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 [Ribo-Seq]

2025-02-01 | GSE274079 | GEO

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 [Ribo-Seq]

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

| PRJNA1144916 | 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]

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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

The METTL5-TRMT112 N6-methyladenosine methyltransferase complex regulates metabolism and development via translation (Identification of m1A mRNA methyltransferase in nucleus by TMT11-LC-MS/MS)

Project description:m1A has long been known to be important in tRNA and rRNA, but we recently mapped many m1A sites in mRNA as well. m1A is found on the 5’ ends of genes, usually around the first splice site, but we have yet to understand how it effects transcript fate. Identifying the methyltransferase would be a major first step towards understanding m1A function.

2021-11-30 | PXD028832 | Pride

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

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