ArticleJournal of experimental & clinical cancer research : CR2023
The N6-methyladenosine METTL3 regulates tumorigenesis and glycolysis by mediating m6A methylation of the tumor suppressor LATS1 in breast cancer.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 126 citations in OpenAlex.
- RBM15B-mediated m6A modification of FOXM1 activates the AURKA/TPX2 axis to promote epithelial-mesenchymal transition-driven endometrial cancer progression.Cell adhesion & migration · 2026Article
- METTL3 promotes proliferation and invasion and inhibits ferroptosis in hepatocellular carcinoma by mediating m6A methylation modification of NUPR1.Molecular and cellular biochemistry · 2026Article
- Inhibiting METTL3 synergizes with Notch blockade to treat ESCC by targeting cancer stemness via m6A-JAG2.Journal of gastroenterology · 2026Article
- N6-methyladenosine-mediated upregulation of PAICS promotes lung-adenocarcinoma metastasis via the integrin-FAK signaling.Oncogene · 2026Article
- The miR-338-5p/METTL3 axis regulates m6A modification to inhibit tumor progression in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- IGF2BP3 Overexpression Accelerates Osteoarthritis Progression by Promoting Glycolysis via mThe Kaohsiung journal of medical sciences · 2026Article
- Integrated multi-omics analysis reveals tumor-suppressive phenotypes and associated transcriptomic remodeling upon METTL3 overexpression in A549 lung cancer cells.Translational cancer research · 2026Article
- METTL3- and IGF2BP1-associated m6A regulation of FADS2 contributes to lipid droplet accumulation and malignant progression in non-small cell lung cancer.Translational cancer research · 2026Article
- Identification of papillary thyroid carcinoma-associated epithelial cell subpopulations and diagnostic biomarkers: integrating machine learning with single-cell analysis.Translational cancer research · 2026Article
- METTL3-mediated m6A modification of CXCR4 drives M2 macrophage polarization and suppresses anti-tumor immunity in esophageal cancer.Journal of clinical biochemistry and nutrition · 2026Article
- METTL3 Potentiates Corneal Allograft Rejection via Increased Pro-Inflammatory Cytokine Production and Aerobic Glycolysis.Investigative ophthalmology & visual science · 2026Article
- The Regulatory Role of mCells · 2026Review
- Lactylation-driven gene signatures define breast cancer prognosis: a predictive model and insights into immune microenvironment dynamics.European journal of medical research · 2026Article
- Intracellular and exosomal miR-101-3p regulated by METTL14 confers Gefitinib sensitivity in NSCLC.Medical oncology (Northwood, London, England) · 2026Article
- RBM15 Enhances 5-Fluorouracil Drug Sensitivity and Suppresses Gastric Cancer Progression by Modulating N6-Methyladenosine Modification of ECT2-Dependent IGF2BP3.Research (Washington, D.C.) · 2026Article
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- m6A-Targeted Cancer Therapy: Molecular Targets, Inhibitors, and Nanodelivery Strategies.International journal of nanomedicine · 2026Review
- Gut Microbiota-induced Long Non-coding RNA Snhg9 Regulates the Development of Human Malignant Tumors.Current molecular medicine · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- METTL3-IGF2BP3 as a glucose sensor in hyperglycemic microenvironment promotes tumorigenesis and glycolysis.International journal of biological sciences · 2026Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundPosttranscriptional modification of tumor-associated factors plays a pivotal role in breast cancer progression. However, the underlying mechanism remains unknown. M6A modifications in cancer cells are dynamic and reversible and have been found to impact tumor initiation and progression through various mechanisms. In this study, we explored the regulatory mechanism of breast cancer cell proliferation and metabolism through m6A methylation in the Hippo pathway.
methodsA combination of MeRIP-seq, RNA-seq and metabolomics-seq was utilized to reveal a map of m6A modifications in breast cancer tissues and cells. We conducted RNA pull-down assays, RIP-qPCR, MeRIP-qPCR, and RNA stability analysis to identify the relationship between m6A proteins and LATS1 in m6A regulation in breast cancer cells. The expression and biological functions of m6A proteins were confirmed in breast cancer cells in vitro and in vivo. Furthermore, we investigated the phosphorylation levels and localization of YAP/TAZ to reveal that the activity of the Hippo pathway was affected by m6A regulation of LATS1 in breast cancer cells.
resultsWe demonstrated that m6A regulation plays an important role in proliferation and glycolytic metabolism in breast cancer through the Hippo pathway factor, LATS1. METTL3 was identified as the m6A writer, with YTHDF2 as the reader protein of LATS1 mRNA, which plays a positive role in promoting both tumorigenesis and glycolysis in breast cancer. High levels of m6A modification were induced by METTL3 in LATS1 mRNA. YTHDF2 identified m6A sites in LATS1 mRNA and reduced its stability. Knockout of the protein expression of METTL3 or YTHDF2 increased the expression of LATS1 mRNA and suppressed breast cancer tumorigenesis by activating YAP/TAZ in the Hippo pathway.
conclusionsIn summary, we discovered that the METTL3-LATS1-YTHDF2 pathway plays an important role in the progression of breast cancer by activating YAP/TAZ in the Hippo pathway.
Indexed as
Identifiers
What Socratic 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 Socratic graph.