ArticleFrontiers in oncology2022
METTL3-Mediated ADAMTS9 Suppression Facilitates Angiogenesis and Carcinogenesis in Gastric Cancer.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Ubiquitin Specific Peptidase 48 Deubiquitinates METTL3 to Modulate Ferroptosis in Gastric Cancer Cells.Molecular carcinogenesis · 2026Article
- Review
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- The role and mechanism of METTL3 in cancer: emerging insights into m6A methylation and therapeutic potential.European journal of medical research · 2025Review
- METTL3-driven m⁶A epigenetics in gastric cancer: unveiling oncogenic networks and clinical translation from tumorigenesis to therapy resistance.Cell biology and toxicology · 2025Review
- Epitranscriptomic alterations induced by environmental toxins: implications for RNA modifications and disease.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.European journal of medical research · 2025Review
- METTL3 stabilizes SERPINE2 via the m6A modification to drive the malignant progression of gastric signet ring cell carcinoma.Translational cancer research · 2025Article
- ADAMTS7 Enhances Gastric Cancer Growth and Metastasis by Triggering the NF-κB Signaling Pathway.Journal of Cancer · 2025Article
- The Mechanism of Sijunzi Decoction Suppresses Gastric Cancer Metastasis via the m6A Methyltransferase METTL14 Based on Untargeted Metabolomics Studies and Network Pharmacology Analysis.Drug design, development and therapy · 2025Article
- Role of N6-methyladenosine RNA modification in cancer.MedComm · 2024Review
- Role of N6-methyladenosine in tumor neovascularization.Cell death & disease · 2024Review
- N6-methyladenosine modification of hypoxia-inducible factor-1α regulatesWorld journal of gastrointestinal oncology · 2024Article
- The regulatory mechanism of m6A modification in gastric cancer.Discover oncology · 2024Review
- METTL14 promotes neuroblastoma formation by inhibiting YWHAH via an m6A-YTHDF1-dependent mechanism.Cell death discovery · 2024Article
- Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis.BMC cancer · 2024Article
- High-Throughput Transcriptomics of Water Extracts Detects Reductions in Biological Activity with Water Treatment Processes.Environmental science & technology · 2024Article
- Regulatory effect of N6-methyladenosine on tumor angiogenesis.Frontiers in immunology · 2024Review
- The role of N6-methyladenosine modification in tumor angiogenesis.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of methyltransferase-like 3 (METTL3), which participates in catalyzing N-methyladenosine (m6A) RNA modification, in gastric cancer (GC) is unclear. Here, we found that METTL3 was overexpressed in human GC. Functionally, we verified that METTL3 promoted tumor cell proliferation and angiogenesis through a series of phenotypic experiments. Subsequently, ADAMTS9 was identified as the downstream effector of METTL3 in GC, which could be degraded by the YTHDF2-dependent pathway. Finally, the data suggested that METTL3 might facilitate GC progression through the ADAMTS9-mediated PI3K/AKT pathway. Our study unveiled the fundamental mechanisms of METTL3 in GC progression. The clinical value of METTL3 in GC deserves further exploration.
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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.