ArticleScience translational medicine2022
Triple-negative breast cancer metastasis involves complex epithelial-mesenchymal transition dynamics and requires vimentin.
Article in Science translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 2 of them syntheses that pooled it.
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Who cites it
132 citing papers in PubMed, 2 syntheses or guidelines pooled it, 180 citations in OpenAlex.
- Comparison of robotic, conventional, and endoscopic nipple-sparing mastectomy with immediate prosthetic breast reconstruction for breast cancer: A systematic review and meta-analysis.Biomolecules & biomedicine · 2025Pooled it
- A systematic review on the culture methods and applications of 3D tumoroids for cancer research and personalized medicine.Cellular oncology (Dordrecht, Netherlands) · 2025Pooled it
- Response to neoadjuvant chemotherapy in early breast cancers is associated with epithelial-mesenchymal transition and tumor-infiltrating lymphocytes.Molecular oncology · 2025Trial
- The tumor microenvironment in triple negative breast cancer and a strategy to improve responses to immunotherapy using cryoablation and immunostimulants.Cancer biology & therapy · 2026Review
- Enhanced anticancer efficacy ofMaterials today. Bio · 2026Article
- MUC1 as a Survival Effector of Radiotherapy-Induced Epithelial Hybrid States in Basal-Like Breast Cancer.International journal of cancer · 2026Article
- Association of Epithelial-to-Mesenchymal Transition Related Markers With Clinical Outcome in Non-Muscle Invasive and Muscle Invasive Bladder Cancer Patients.Cell biochemistry and biophysics · 2026Article
- Epithelial-mesenchymal transition in carcinoma: navigating phenotypic states to target resistance and metastasis.Cancer metastasis reviews · 2026Review
- Distinct metabolic dependency on BCAA defines cancer stemness and malignancy in human triple-negative breast cancer.Cell reports · 2026Article
- Multiple distinct metastatic cell states are induced by epithelial-mesenchymal plasticity.bioRxiv : the preprint server for biology · 2026Article
- Keratin 6A Overexpression in the Lymphovascular Invasion-Associated Tumor Subgroup Promotes Progression of Triple-Negative Breast Cancer.Cancer research and treatment · 2026Article
- Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer.Molecular therapy. Nucleic acids · 2026Article
- PRMT5/Sohlh2/Sirt1 Signaling Pathway in Vascular Endothelial Cells Modulates Lung Metastasis of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sequential invasion assays identify carbonic anhydrase IX as a driver of invasiveness in epithelial triple-negative breast cancer cells.American journal of physiology. Cell physiology · 2026Article
- Targeting arginine metabolism reverses bone immunosuppressive microenvironment and metastasis in ARID1A-deficient triple negative breast cancer.Nature communications · 2026Article
- Sorbicillin water fraction from Penicillium flavigenum: Impact on anti-proliferative, apoptotic, and neuroinflammatory responses in glioma model.Molecular biology reports · 2026Article
- N-Orbit: towards a universal model and metric for comparing tissue microenvironments.Nature communications · 2026Article
- Single-cell morphodynamical trajectories enable prediction of gene expression accompanying cell state change.Cell systems · 2026Article
- Micropeptide SCAPEP triggers lung adenocarcinoma tumorigenesis via regulating autophagy by promoting CDK15-mediated phosphorylation of vimentin.Cell death & disease · 2026Article
- NRG4 suppresses breast cancer metastasis via ERBB4-YAP1-mediated down-regulation of MMPs.Genes & diseases · 2026Article
72 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive subtype associated with early metastatic recurrence and worse patient outcomes. TNBC tumors express molecular markers of the epithelial-mesenchymal transition (EMT), but its requirement during spontaneous TNBC metastasis in vivo remains incompletely understood. We demonstrated that spontaneous TNBC tumors from a genetically engineered mouse model (GEMM), multiple patient-derived xenografts, and archival patient samples exhibited large populations in vivo of hybrid E/M cells that lead invasion ex vivo while expressing both epithelial and mesenchymal characteristics. The mesenchymal marker vimentin promoted invasion and repressed metastatic outgrowth. We next tested the requirement for five EMT transcription factors and observed distinct patterns of utilization during invasion and colony formation. These differences suggested a sequential activation of multiple EMT molecular programs during the metastatic cascade. Consistent with this model, our longitudinal single-cell RNA analysis detected three different EMT-related molecular patterns. We observed cancer cells progressing from epithelial to hybrid E/M and strongly mesenchymal patterns during invasion and from epithelial to a hybrid E/M pattern during colony formation. We next investigated the relative epithelial versus mesenchymal state of cancer cells in both GEMM and patient metastases. In both contexts, we observed heterogeneity between and within metastases in the same individual. We observed a complex spectrum of epithelial, hybrid E/M, and mesenchymal cell states within metastases, suggesting that there are multiple successful molecular strategies for distant organ colonization. Together, our results demonstrate an important and complex role for EMT programs during TNBC metastasis.
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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.