ArticleNature communications2025
L3MBTL3 and STAT3 collaboratively upregulate SNAIL expression to promote metastasis in female breast cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Exosome-Transferred STAT3 from Cancer-Associated Fibroblasts Expedites Thymic Carcinoma Malignant Progression and M2 Macrophage Polarization Through Transcriptionally Activating KLHL5.Applied biochemistry and biotechnology · 2026Article
- Epithelial-mesenchymal transition and sunitinib resistance in renal cell carcinoma: mechanisms and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Renal insulin-like growth factor binding-protein 7 is a critical promoter of progressive diabetic kidney disease.Nature communications · 2025Article
- Cancer stem cells and Lon-noncRNA promotes invasion, metastasis and tumor growth in breast cancer through regulation of signaling pathway.Scientific reports · 2025Article
- Transcriptomic and Functional Validation Reveals PAQR3/P6-55 as Potential Therapeutic Targets in Colon Cancer.Biology · 2025Article
- Irisin's Dual Role in Malignant Tumors and Its Potential as a Biomarker and Therapeutic Target.Drug design, development and therapy · 2025Review
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Authors and funding
14 authors.
Funding
Abstract
The STAT3 pathway promotes epithelial-mesenchymal transition, migration, invasion and metastasis in cancer. STAT3 upregulates the transcription of the key epithelial-mesenchymal transition transcription factor SNAIL in a DNA binding-independent manner. However, the mechanism by which STAT3 is recruited to the SNAIL promoter to upregulate its expression is still elusive. In our study, the lysine methylation binding protein L3MBTL3 is positively associated with metastasis and poor prognosis in female patients with breast cancer. L3MBTL3 also promotes epithelial-mesenchymal transition and metastasis in breast cancer. Mechanistic analysis reveals that L3MBTL3 interacts with STAT3 and recruits STAT3 to the SNAIL promoter to increase SNAIL transcription levels. The interaction between L3MBTL3 and STAT3 is required for SNAIL transcription upregulation and metastasis in breast cancer, while the methylated lysine binding activity of L3MBTL3 is not required for these functions. In conclusion, L3MBTL3 and STAT3 synergistically upregulate SNAIL expression to promote breast cancer metastasis.
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