ArticleEMBO reports2023
METTL14 modulates glycolysis to inhibit colorectal tumorigenesis in p53-wild-type cells.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 62 citations in OpenAlex.
- METTL14-Mediated lncRNA MSTRG.292666.16 mInternational journal of molecular sciences · 2026Article
- GDPPH1 induces cell cycle arrest by downregulation of CDK4/Cyclin D1 via the mCell death & disease · 2026Article
- Matrine functions as a tumor inhibitor to influence proliferation, metastasis and glycolysis in colorectal cancer via depending on METTL14-mediated m6A methylation of MEX3A.Molecular and cellular biochemistry · 2026Article
- REEP6 promotes colorectal cancer glycolysis and tumorigenesis through PRMT5-mediated PGAM1 arginine methylation.Acta pharmaceutica Sinica. B · 2026Article
- Identification and Experimental Verification Reveal SLC2A3 Associated With Prognosis and Immune Infiltration in Colon Adenocarcinoma.Mediators of inflammation · 2026Article
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- Berberine restrains the expansion of colorectal cancer organoids by blocking cell cycle progression and reducing lipid synthesis.Frontiers in immunology · 2026Article
- Crosstalk between mFrontiers in immunology · 2026Review
- Development and Validation of an m6A-Derived Prognostic Signature in Lung Adenocarcinoma.Journal of Cancer · 2026Article
- Influence of RNA Modifications on Cancer Metabolism: Interplay with Hypoxia and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Review
- METTL14 MediatesRedox report : communications in free radical research · 2025Article
- 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
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- METTL14 induces ferroptosis to inhibit colorectal cancer progression by inhibiting TRIB3 via an m6A-YTHDF2-dependent manner.Journal of molecular histology · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- METTL3 mediates m6A methylation modification of ULBP2 and affects the progression of cervical cancer.Hereditas · 2025Article
- ZNF384 mediates KRT23 to promote CRC process through the TGF-β/Smad signaling pathway.Cytotechnology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
The frequency of p53 mutations in colorectal cancer (CRC) is approximately 40-50%. A variety of therapies are being developed to target tumors expressing mutant p53. However, potential therapeutic targets for CRC expressing wild-type p53 are rare. In this study, we show that METTL14 is transcriptionally activated by wild-type p53 and suppresses tumor growth only in p53-wild-type (p53-WT) CRC cells. METTL14 deletion promotes both AOM/DSS and AOM-induced CRC growth in mouse models with the intestinal epithelial cell-specific knockout of METTL14. Additionally, METTL14 restrains aerobic glycolysis in p53-WT CRC, by repressing SLC2A3 and PGAM1 expression via selectively promoting m
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.