ArticleMolecular oncology2021
METTL3/YTHDF2 m6A axis accelerates colorectal carcinogenesis through epigenetically suppressing YPEL5.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
60 citing papers in PubMed, 85 citations in OpenAlex.
- Single-cell transcriptomic profiling combined with Mendelian randomization illuminates molecular drivers of bladder cancer.Molecular genetics and genomics : MGG · 2026Article
- YPEL1 Inhibits Development of Gemcitabine Resistance in NK / T Cell Lymphomas.Current cancer drug targets · 2026Article
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 2025Review
- METTL3 in colorectal cancer: molecular insights and clinical implications.Molecular biology reports · 2025Review
- The many faces of the GID/CTLH E3 ligase complex.Biochemical Society transactions · 2025Review
- Pleckstrin-2 promotes the progression of colorectal cancer via YTHDF2-mediated TYMS mRNA stability.Cellular and molecular life sciences : CMLS · 2025Article
- Switching from messenger RNAs to noncoding RNAs,World journal of gastrointestinal oncology · 2025Review
- METTL3 Promotes OSCC Progression by Down-Regulating WEE1 in a m6A-YTHDF2-Dependent Manner.Molecular biotechnology · 2025Article
- METTL3, an Independent Adverse Prognostic Factor for AML, Promotes the Development of AML by Modulating the PGC-1α-MAPK Pathway and PGC-1α-Antioxidant System Axis.Cancer medicine · 2025Article
- YTHDC1 negatively regulates UBE3A to influence RAD51 ubiquitination and inhibit apoptosis in colorectal cancer cells.Scientific reports · 2025Article
- RBM15B Promotes Prostate Cancer Cell Proliferation via PCNA m6A Modification.Cell biochemistry and biophysics · 2025Article
- The METTL3/TRAP1 axis as a key regulator of 5-fluorouracil chemosensitivity in colorectal cancer.Molecular and cellular biochemistry · 2025Article
- N6-methyladenosine (m6A)-forming enzyme METTL3 controls UAF1 stability to promote inflammation in a model of colitis by stimulating NLRP3.Scientific reports · 2025Article
- METTL3‑mediated N6‑methyladenosine modification of MMP9 mRNA promotes colorectal cancer proliferation and migration.Oncology reports · 2025Article
- Metabolism and epigenetics in cancer: toward personalized treatment.Frontiers in endocrinology · 2025Review
- RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy.Molecular cancer · 2024Review
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Role of N6-methyladenosine RNA modification in cancer.MedComm · 2024Review
- Intracellular Fusobacterium nucleatum infection increases METTL3-mediated m6A methylation to promote the metastasis of esophageal squamous cell carcinoma.Journal of advanced research · 2024Article
- Non-canonical substrate recognition by the human WDR26-CTLH E3 ligase regulates prodrug metabolism.Molecular cell · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
N6-methyladenosine (m6A) has emerged as the most prevalent post-transcriptional modification on mRNA that contributes prominently to tumorigenesis. However, the specific function of m6A methyltransferase methyltransferase-like 3 (METTL3) in colorectal cancer (CRC) remains elusive. Herein, we explored the biological function of METTL3 in CRC progression. Clinically, METTL3 was frequently upregulated in CRC tissues, cell lines, and plasma samples and its high expression predicted poor prognosis of CRC patients. Functionally, knockdown of METTL3 significantly repressed CRC cell proliferation and migration in vitro, while its overexpression accelerated CRC tumor formation and metastasis both in vitro and in vivo. Mechanistically, METTL3 epigenetically repressed YPEL5 in an m6A-YTHDF2-dependent manner by targeting the m6A site in the coding sequence region of the YPEL5 transcript. Moreover, overexpression of YPEL5 significantly reduced CCNB1 and PCNA expression. Collectively, we identified the pivotal role of METTL3-catalyzed m6A modification in CRC tumorigenesis, wherein it facilitates CRC tumor growth and metastasis through suppressing YPEL5 expression in an m6A-YTHDF2-dependent manner, suggesting a promising strategy for the diagnosis and therapy of CRC.
Indexed as
Identifiers
What OpenQuestion holds
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.