ArticleJournal of Cancer2023
Suppression of Wnt/β-catenin Signaling in PDAC via METTL16-mediated N6-methyladenosine Modification of DVL2.
Article in Journal of Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- The methyltransferase METTL16 in digestive system cancers: functions and mechanisms.Frontiers in oncology · 2026Review
- Role of m6A RNA methylation regulators in pancreatic cancer: interactions and potential implications.Cancer cell international · 2025Review
- Recent Findings in N6-Methyladenosine Modification and Significance in Pancreatic Cancer.Cancer medicine · 2025Review
- RNA mCell investigation · 2025Article
- METTL16 emerges as a pivotal epitranscriptomic regulator, linking RNA modification, tumor progression, and immune modulation.Frontiers in immunology · 2025Review
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- The Roles and Implications of m6A Methylation in Radiotherapy for Gastrointestinal Tumors.Dose-response : a publication of International Hormesis SocietyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer is a formidable cause of cancer-related deaths worldwide and has witnessed a more than twofold increase in incidence over the last 25 years. The most frequently occurring form of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC), accounting for the majority of pancreatic cancer cases. N6-methyladenosine (m6A), the most abundant transcript modification, has been implicated in the pathogenesis of numerous human cancers, including pancreatic cancer. Despite this, the functional role of methyltransferase-like 16 (METTL16), a critical m6A methyltransferase, in PDAC remains elusive. In this study, we demonstrate that METTL16 expression is significantly diminished in PDAC, rendering it a promising prognostic indicator. Strikingly, both in vitro and in vivo assays revealed accelerated metastasis and invasion of PDAC cells upon METTL16 knockdown, while overexpression of METTL16 exerted an opposite effect. Mechanistically, METTL16 regulates DVL2 expression by suppressing its translation via m
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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.