ArticleJournal of cancer research and clinical oncology2023
METTL3 promotes colorectal cancer metastasis by promoting the maturation of pri-microRNA-196b.
Article in Journal of cancer research and clinical oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- METTL3 in colorectal cancer: molecular insights and clinical implications.Molecular biology reports · 2025Review
- MicroRNA Let-7b-5p Targets IGF1R to Inhibit the Progression of Hepatocellular Carcinoma Through the AKT/mTOR Pathway.Cancer medicine · 2025Article
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Cancer-associated fibroblast-derived exosomal FAM83F regulates KIF23 expression to promote the malignant progression and reduce radiosensitivity in non-small cell lung cancer.Cytotechnology · 2025Article
- Recent advances in noncoding RNA modifications of gastrointestinal cancer.Cancer science · 2025Review
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024Review
- Targeting key RNA methylation enzymes to improve the outcome of colorectal cancer chemotherapy (Review).International journal of oncology · 2024Review
- The METTL3/miR-196a Axis Predicts Poor Prognosis in Non-small Cell Lung Cancer.Journal of Cancer · 2024Article
- Methyltransferase-like proteins in cancer biology and potential therapeutic targeting.Journal of hematology & oncology · 2023Review
- The bidirectional interplay between ncRNAs and methylation modifications in gastrointestinal tumors.International journal of biological sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
purposeMethyltransferase-like 3 (METTL3), a key member of the m6A methyltransferase complex, is upregulated in multiple human malignancies and plays a role in regulating tumor migration. This study aimed to reveal the underlying mechanism by which METTL3 in regulates the metastasis of colorectal cancer (CRC).
methodsWe compared METTL3 expression levels in CRC tumor tissues and adjacent nontumor tissues by immunohistochemistry (IHC). The functional roles of METTL3 in CRC were assessed by real-time cell migration assays, wound-healing assays and Transwell assays. miRNA sequencing (miRNA-seq), RNA-binding protein immunoprecipitation (RIP) assays and N6-methyladenosine immunoprecipitation (MeRIP) assays were performed to confirm the molecular mechanism underlying the involvement of METTL3 in CRC cell metastasis.
resultsWe found that METTL3 was overexpressed in CRC tissues. METTL3 knockdown significantly inhibited CRC cell migration and invasion, while METTL3 overexpression had the opposite effects. Furthermore, we demonstrated that METTL3 regulates miR-196b expression via an N6-methyladenosine (m6A)-pri-miR-196b-dependent mechanism and thereby promotes CRC metastasis.
conclusionThis study shows the important role of METTL3 in CRC metastasis and provides novel insight into m6A modification in CRC metastasis.
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