ArticleCellular oncology (Dordrecht, Netherlands)2026
METTL1-mediated m
Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Hyperglycemia-driven metabolic memory signaling destabilizes METTL1 to trigger inflammatory hypertrophy and fibrosis in diabetic cardiomyopathy.Acta diabetologica · 2026Article
- Hyperglycemia-driven metabolic memory signaling destabilizes METTL1 to trigger inflammatory hypertrophy and fibrosis in diabetic cardiomyopathy.Acta diabetologica · 2026Article
- N7-Methylguanosine Modification in Colorectal Cancer: Molecular Insights and Clinical Implications.International journal of molecular sciences · 2026Review
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Authors and funding
14 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with colorectal cancer liver metastasis (CRLM) being the primary cause of death. Despite its clinical significance, the molecular mechanisms underlying CRC progression remain poorly understood.
methodsUnbiased proteomic profiling and single-cell RNA sequencing (scRNA-seq) analyses of CRC tissues from patients with and without liver metastases identified methyltransferase-like protein 1 (METTL1) as a critical regulator, with its function in CRC progression validated through in vitro and in vivo gain- and loss-of-function studies. Furthermore, tRNA methylation sequencing (TRAC-seq) and ribosome-nascent chain complex sequencing (RNC-seq) were performed to investigate the downstream mechanisms.
resultsMETTL1 was significantly elevated in CRC, with the highest expression in CRLM, and correlated with poor survival. METTL1 knockout inhibited tumor cell proliferation, migration, and invasion in vitro, whereas overexpression of wild-type METTL1, but not its catalytically inactive mutant, promoted oncogenic phenotypes. Consistently, METTL1 knockout attenuated tumor growth and liver metastasis in vivo. Mechanistically, METTL1-mediated m7G tRNA modification selectively enhanced translation of oncogenic transcripts, particularly those involved in cell cycle regulation (e.g., CCND3) and PI3K/Akt signaling. Notably, forced CCND3 expression partially rescued the phenotypes induced by METTL1 knockout.
conclusionsOur findings highlight the crucial role of METTL1 and its tRNA m7G modification in promoting CRC progression and liver metastasis, providing promising targets for therapy in advanced CRC.
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