ArticleCell proliferation2024
YTHDF1 mediates N-methyl-N-nitrosourea-induced gastric carcinogenesis by controlling HSPH1 translation.
Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- Construction and evaluation of an independently generated transgenic mouse model carrying mutated human HRAS genes for short-term carcinogenicity assessment.Transgenic research · 2026Article
- YTHDF3 Promotes the Progression of Gastric Cancer by Activating the Wnt/β-Catenin Signaling Pathway via Targeting NEK7.Journal of gastroenterology and hepatology · 2026Article
- Single-cell and bulk omics uncover fibroblast heterogeneity and HSPH1 as a key driver in Barrett's esophagus to esophageal adenocarcinoma progression.Cancer cell international · 2026Article
- mActa pharmaceutica Sinica. B · 2025Review
- Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.European journal of medical research · 2025Review
- The Toxicity of Dimethyl Sulfoxide Combined with the Alkylating Agent MNU on Mice: Focusing on Mortality and Activity Impairment.Drug design, development and therapy · 2025Article
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
- Classical biomarkers and non-coding RNAs associated with diagnosis and treatment in gastric cancer.Oncology research · 2025Review
- Epigenetic regulation of RNA methylations in gastric cancer.Oncology reviews · 2025Review
- Prediction of neoadjuvant therapy efficacy in gastric cancer: the interplay between biomarkers and radiomics and its potential for clinical translation.Frontiers in oncology · 2025Review
- The Pivotal Role of Preclinical Animal Models in Anti-Cancer Drug Discovery and Personalized Cancer Therapy Strategies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The YTH domain-containing protein family: Emerging players in immunomodulation and tumour immunotherapy targets.Clinical and translational medicine · 2024Review
- YTHDF1 mediates N-methyl-N-nitrosourea-induced gastric carcinogenesis by controlling HSPH1 translation.Cell proliferation · 2024Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
YT521-B homology (YTH) domain family (YTHDF) proteins serve as readers that directly recognise m6A modifications. In this study, we aim to probe the role of YTHDF1 in environmental carcinogen-induced malignant transformation of gastric cells and gastric cancer (GC) carcinogenesis. We established a long-term low-dose MNU-induced malignant transformation model in gastric epithelial cells. In vivo and in vitro experiments were conducted to validate the malignant phenotype and characterise the roles of YTHDF1 and its downstream genes in malignant transformation cells. Additionally, we explored downstream m6A modification targets of YTHDF1 using RNA-sequencing, RNA immunoprecipitation, and proteomics analyses, and conducted validation experiments in cell experiments and clinical samples. Long-term low-dose exposure of MNU converted normal Gges-1 cells into malignant cells. YTHDF1 mRNA and protein expression are increased in MNU-induced malignant cells (p<0.001). Meanwhile, YTHDF1 knockdown inhibits the malignant potential of MNU-treated cells (p<0.01). YTHDF1 knockdown specifically suppresses HSPH1 protein, but not RNA levels. RIP-qPCR validates HSPH1 is the target of YTHDF1 (p<0.01). HSPH1 knockdown impairs the malignant potential of MNU-induced transformed cells. The increased expression of the key regulatory factor YTHDF1 in MNU-induced gastric carcinogenesis affects malignant transformation and tumorigenesis by regulating the translation of downstream HSPH1. These findings provide new potential targets for preventing and treating environmental chemical-induced gastric carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.