ArticleJournal of cellular and molecular medicine2024
METTL14/miR-29c-3p axis drives aerobic glycolysis to promote triple-negative breast cancer progression though TRIM9-mediated PKM2 ubiquitination.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway.Translational cancer research · 2026Article
- mFrontiers in cell and developmental biology · 2026Review
- USP5 promotes glycolysis of fibroblast-like synoviocytes by stabilizing the METTL14/mCell death discovery · 2025Article
- Ubiquitin-specific protease 7 regulates macrophage polarization via pyruvate kinase M2-mediated metabolic reprogramming in severe acute pancreatitis.Cell death & disease · 2025Article
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Exosome-delivered METTL14 drives hypoxia-induced proliferation, metastasis, and glycolysis of breast cancer cells through regulating TRIM16-mediated FGF7 ubiquitination.Breast cancer research : BCR · 2025Article
- Post-translational modifications and the reprogramming of tumor metabolism.Discover oncology · 2025Review
- Oxidative phosphorylation-related genes for prognosis and tumor microenvironment in breast cancer.Translational cancer research · 2025Article
- Exosomal miR-21-5p from glioma associated mesenchymal stem cells promotes the progression and glycolysis of glioblastoma via PDHA1.Scientific reports · 2025Article
- Emerging Roles of ncRNAs Regulating PKM2 in Cancer Progression.Current pharmaceutical biotechnology · 2025Review
- PKM2-driven metabolic reprogramming in digestive system tumors: mechanisms, therapeutic advances, and clinical challenges.Frontiers in immunology · 2025Review
- The inspiration of methyltransferase in RNA methylation modification for targeted therapy of malignant tumors.Frontiers in immunology · 2025Review
- Multifaceted role ofMedComm · 2024Review
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- METTL14/miR-29c-3p axis drives aerobic glycolysis to promote triple-negative breast cancer progression though TRIM9-mediated PKM2 ubiquitination.Journal of cellular and molecular medicine · 2024Article
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5 authors.
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Abstract
The energy metabolic rearrangement of triple-negative breast cancer (TNBC) from oxidative phosphorylation to aerobic glycolysis is a significant biological feature and can promote the malignant progression. However, there is little knowledge about the functional mechanisms of methyltransferase-like protein 14 (METTL14) mediated contributes to TNBC malignant progression. Our study found that METTL14 expression was significantly upregulated in TNBC tissues and cell lines. Silencing METTL14 significantly inhibited TNBC cell growth and invasion in vitro, as well as suppressed tumour growth. Mechanically, METTL14 was first found to activate miR-29c-3p through m6A and regulate tripartite motif containing 9 (TRIM9) to promote ubiquitination of pyruvate kinase isoform M2 (PKM2) and lead to its transition from tetramer to dimer, resulting in glucose metabolic reprogramming from oxidative phosphorylation to aerobic glycolysis to promote the progress of TNBC. Taken together, these findings reveal important roles of METTL14 in TNBC tumorigenesis and energy metabolism, which might represent a novel potential therapeutic target for TNBC.
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