ArticleJournal of experimental & clinical cancer research : CR2022
METTL3 promotes colorectal carcinoma progression by regulating the m6A-CRB3-Hippo axis.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- mNature communications · 2026Article
- The PRKN/METTL3/CLDN2 axis promotes colorectal cancer development through epigenetic mechanisms.Cell biology and toxicology · 2026Article
- NNature reviews. Cancer · 2026Review
- METTL16 antagonizes astaxanthin-induced ferroptosis in colorectal cancer cells.Translational cancer research · 2026Article
- The Regulatory Role of mCells · 2026Review
- Preparation and Antitumor Activity of METTL3 SiRNA Nanoparticles Carried by Hypoxia Sensitive Polymer (mPEG-Azo-PEI).International journal of nanomedicine · 2026Article
- Epigenetic and mitoepigenetic regulation in cancer and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- METTL3 promotes chondrocyte injury in osteoarthritis by increasing CTSB expression.Journal of orthopaedic surgery and research · 2025Article
- Review
- A multi-omic integrative approach combining mGenes & diseases · 2025Article
- Machine learning-based model identifies a novel cuproptosis-related mitochondrial gene signature with a key role in the prognosis and treatment of lung adenocarcinoma.Oncology letters · 2025Article
- The effects of genetically determined plasma methyltransferases on digestive system cancers: a comprehensive bidirectional two-sample Mendelian randomization analysis.Discover oncology · 2025Article
- Integrative multiomic and immune profiling of lung adenocarcinoma: molecular landscapes, gene expression, and treatment response insights.The oncologist · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- METTL3 and METTL14 drive pancreatic adenocarcinoma progression via m6A-dependent alternative splicing in PANC-1 cells.Discover oncology · 2025Article
- METTL3 promotes peritoneal metastasis of colorectal cancer through regulating m6A modification of NRXN3 mRNA.iScience · 2025Article
- HNRNPC stabilizes m6A-modified AC145207.5 to accelerate tumorigenesis in colorectal cancer by impeding the Nrf2/GPX4 axis-mediated ferroptosis.Non-coding RNA research · 2025Article
- SSB cooperates with METTL16-mediated mCell reports · 2025Article
- O-GlcNAcylation of METTL3 drives hepatocellular carcinoma progression by upregulating MCM10 expression in an m6A-IGF2BP3-dependent manner.Cell death & disease · 2025Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundColorectal carcinoma (CRC) is the third most common cancer and second most common cause of cancer-related deaths worldwide. Ribonucleic acid (RNA) N6-methyladnosine (m6A) and methyltransferase-like 3 (METTL3) play key roles in cancer progression. However, the roles of m6A and METTL3 in CRC progression require further clarification.
methodsAdenoma and CRC samples were examined to detect m6A and METTL3 levels, and tissue microarrays were performed to evaluate the association of m6A and METTL3 levels with the survival of patients with CRC. The biological functions of METTL3 were investigated through cell counting kit-8, wound healing, and transwell assays. M6A epitranscriptomic microarray, methylated RNA immunoprecipitation-qPCR, RNA stability, luciferase reporter, and RNA immunoprecipitation assays were performed to explore the mechanism of METTL3 in CRC progression.
resultsM6A and METTL3 levels were substantially elevated in CRC tissues, and patients with CRC with a high m6A or METTL3 levels exhibited shorter overall survival. METTL3 knockdown substantially inhibited the proliferation, migration, and invasion of CRC cells. An m6A epitranscriptomic microarray revealed that the cell polarity regulator Crumbs3 (CRB3) was the downstream target of METTL3. METTL3 knockdown substantially reduced the m6A level of CRB3, and inhibited the degradation of CRB3 mRNA to increase CRB3 expression. Luciferase reporter assays also showed that the transcriptional level of wild-type CRB3 significantly increased after METTL3 knockdown but not its level of variation. Knockdown of YT521-B homology domain-containing family protein 2 (YTHDF2) substantially increased CRB3 expression. RNA immunoprecipitation assays also verified the direct interaction between the YTHDF2 and CRB3 mRNA, and this direct interaction was impaired after METTL3 inhibition. In addition, CRB3 knockdown significantly promoted the proliferation, migration, and invasion of CRC cells. Mechanistically, METTL3 knockdown activated the Hippo pathway and reduced nuclear localization of Yes1-associated transcriptional regulator, and the effects were reversed by CRB3 knockdown.
conclusionsM6A and METTL3 levels were substantially elevated in CRC tissues relative to normal tissues. Patients with CRC with high m6A or METTL3 levels exhibited shorter overall survival, and METTL3 promoted CRC progression. Mechanistically, METTL3 regulated the progression of CRC by regulating the m6A-CRB3-Hippo pathway.
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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.