ArticleOncogene2009
Interleukin-6 induces an epithelial-mesenchymal transition phenotype in human breast cancer cells.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 421 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
421 citing papers in PubMed, 1 synthesis or guideline pooled it, 749 citations in OpenAlex.
- The Role of Cytokines in Epithelial-Mesenchymal Transition in Gynaecological Cancers: A Systematic Review.Cells · 2023Pooled it
- Interaction Between SNP Genotype and Efficacy of Anastrozole and Exemestane in Early-Stage Breast Cancer.Clinical pharmacology and therapeutics · 2021Trial
- Effect of Indirect Co-Culture With Gingival Mesenchymal Stem Cells on Cytokine Secretion in Primary Oral Squamous Cell Carcinoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Review
- Homeobox A10 in gastrointestinal malignancies: unraveling metastatic mechanisms and novel therapeutic opportunities.Cancer metastasis reviews · 2026Review
- Employing a Combination of Chemoattractants to Trap Glioblastoma Cells in a Macroporous Hydrogel.Pharmaceutics · 2026Article
- JAK inhibition in PD-1 immunotherapy and tumor microenvironment.Frontiers in immunology · 2026Review
- Temporal Trends in Vulvar Cancer Cases and Associated Factors of Adverse Clinical Features: A 6-year Retrospective Study From a Tertiary Hospital in Indonesia.International journal of women's health · 2026Article
- UNC93B1 drives IL-6/STAT3-dependent tumor-macrophage crosstalk and epithelial-mesenchymal transition in breast cancer.Frontiers in pharmacology · 2026Article
- Cancer-associated fibroblast-derived interleukin-6 as a key driver of epithelial-mesenchymal transition and metastasis in oral squamous cell carcinoma.Journal of dental sciences · 2026Article
- Transcriptome study exploring the mechanisms linking pollutants and breast cancer aggressiveness.Scientific reports · 2025Article
- Epithelial-Mesenchymal Transition in Human Alveolar Cells Exposed to Indium Chloride.Journal of applied toxicology : JAT · 2025Article
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.Cancer cell international · 2025Review
- Cardiometabolic disease and cardio-oncology: Insights from iPSC models and tissue engineering.Cell reports. Medicine · 2025Review
- Tumor-expressed GPNMB orchestrates Siglec-9Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6/JAK2/STAT3 Axis in Pancreatic Cancer.Cancer medicine · 2025Article
- POC1A induces epithelial-mesenchymal transition to promote growth and metastasis through the STAT3 signaling pathway in triple-negative breast cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Inhibitory Impact of the Amino Benzoic Derivative DAB-2-28 on the Process of Epithelial-Mesenchymal Transition in Human Breast Cancer Cells.Molecules (Basel, Switzerland) · 2025Article
361 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Breast tumor interleukin-6 (IL-6) levels increase with tumor grade, and elevated serum IL-6 correlates with poor breast cancer patient survival. Epithelial-mesenchymal transition (EMT) phenotypes such as impaired E-cadherin expression or aberrant Vimentin induction are associated with enhanced metastasis and unfavorable clinical outcome in breast cancer. Despite this fact, few tumor microenvironment-derived extracellular signaling factors capable of provoking such a phenotypic transition have been identified. In this study, we showed that IL-6 promoted E-cadherin repression among a panel of estrogen receptor-alpha-positive human breast cancer cells. Furthermore, ectopic stable IL-6 expressing MCF-7 breast adenocarcinoma cells (MCF-7(IL-6)) exhibited an EMT phenotype characterized by impaired E-cadherin expression and induction of Vimentin, N-cadherin, Snail and Twist. MCF-7(IL-6) cells formed xenograft tumors that displayed loss of E-cadherin, robust Vimentin induction, increased proliferative indices, advanced tumor grade and undifferentiated histology. Finally, we showed aberrant IL-6 production and STAT3 activation in MCF-7 cells that constitutively express Twist, a metastatic regulator and direct transcriptional repressor of E-cadherin. To our knowledge, this is the first study that shows IL-6 as an inducer of an EMT phenotype in breast cancer cells and implicates its potential to promote breast cancer metastasis.
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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.