ArticleCancer cell international2021
The m6A methyltransferase METTL3 controls epithelial-mesenchymal transition, migration and invasion of breast cancer through the MALAT1/miR-26b/HMGA2 axis.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 81 citations in OpenAlex.
- mExperimental and therapeutic medicine · 2026Review
- 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
- Methylation marks breast cancer metastasis: The roles of mThe Journal of biological chemistry · 2026Review
- METTL3-mediated mJournal of translational medicine · 2026Article
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- Functional and clinical significance of the RNA mNPJ breast cancer · 2025Article
- HOTAIR requires epitranscriptomic modification to exert its pivotal epigenetic role in Epithelial to Mesenchymal Transition.Cell death & disease · 2025Article
- mMolecules (Basel, Switzerland) · 2025Review
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Regulatory role of the METTL3/MALAT1 axis in multiple myeloma progression.Journal of bone oncology · 2025Article
- LncRNA-Protein Interactions: A Key to Deciphering LncRNA Mechanisms.Biomolecules · 2025Review
- Article
- Interactions between long non-coding RNAs and m6 A modification in cancer.Discover oncology · 2025Review
- Epigenetic and epitranscriptomic role of lncRNA in carcinogenesis (Review).International journal of oncology · 2025Review
- Article
- Crosstalk Between m6A RNA Methylation and miRNA Biogenesis in Cancer: An Unholy Nexus.Molecular biotechnology · 2024Review
- Dynamic RNA methylation modifications and their regulatory role in mammalian development and diseases.Science China. Life sciences · 2024Review
- Functions and mechanisms of RNA mInternational journal of oncology · 2024Review
- Functions of methyltransferase-like 3 in breast cancer: pathogenesis, drug resistance, and therapeutic target.Breast cancer research : BCR · 2024Review
1 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies have revealed the key functions of N6-methyladenosine (m6A) modification in breast cancer (BC). MALAT1 as a highly m6A modified lncRNA associated with cancer development and metastasis, but the functional relevance of m6A methyltransferase and MALAT1 in BC is still unknown. Here, our study investigated the effects of the novel m6A methyltransferase METTL3 on epithelial-mesenchymal transition (EMT) in BC via the MALAT1/miR-26b/HMGA2 axis.
methodsFirstly, we collected clinical BC samples and cultured BC cells, and detected mRNA and protein levels in the human samples and human cell lines by RT-qPCR and Western blot, respectively. Then, the binding of MALAT1 and miR-26b and the targeting relationship between miR-26b and HMGA2 were examined by dual-luciferase assay. Moreover, the binding of MALAT1 and miR-26b was tested by RNA pull down and RNA immunoprecipitation (RIP) assays. Methylated-RNA immunoprecipitation (Me-RIP) was used to detect the m6A modification level of MALAT1. The interaction of METTL3 and MALAT1 was detected by photoactivatable ribonucleoside-crosslinking immunoprecipitation (PAR-CLIP). Finally, effects on invasion and migration were detected by Transwell.
resultsIn BC, the level of miR-26b was consistently low, while the levels of METTL3, MALAT1 and HMGA2 were high. Further experiments showed that METTL3 up-regulated MALAT1 expression by modulating the m6A modification of MALAT1, and that MALAT1 could promote the expression of HMGA2 by sponging miR-26b. In BC cells, we found that silencing METTL3 could inhibit EMT and tumor cell invasion by suppressing MALAT1. Furthermore, MALAT1 mediated miR-26b to target HMGA2 and promote EMT, migration, and invasion. In summary, METTL3 promoted tumorigenesis of BC via the MALAT1/miR-26b/HMGA2 axis.
conclusionsSilencing METTL3 down-regulate MALAT1 and HMGA2 by sponging miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC.
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