ArticleOncogene2016
TGF-β1-induced EMT promotes targeted migration of breast cancer cells through the lymphatic system by the activation of CCR7/CCL21-mediated chemotaxis.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.
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Who cites it
179 citing papers in PubMed.
- Multi-omic analysis of the liver-breast axis reveals key hepatic mediators of breast cancer progression.Science China. Life sciences · 2026Review
- Podoplanin-defined tumour plasticity and CCR7-mediated lymphatic metastasis in triple-negative breast cancer.British journal of cancer · 2026Article
- TGF-α/EGFR-mediated lymphatic metastasis reveals a repositionable therapeutic target in breast cancer.NPJ breast cancer · 2026Article
- LMO2 Regulates Epithelial-Mesenchymal Plasticity of Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2026Article
- Multiomic profiling of ER-positive HER2-negative breast cancer reveals markers associated with metastatic spread.Breast cancer research : BCR · 2026Observational
- Reshaping cancer cell plasticity by P-body dynamics and protein translation.Communications biology · 2026Review
- TGF-β in hematologic malignancies: molecular functions and clinical applications.Frontiers in immunology · 2026Review
- Diversified, endothelial cell-dependent cancer cell response to hypertensive serum modified by antihypertensive drugs.Scientific reports · 2025Article
- Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.Cancer cell international · 2025Review
- Suppression of breast cancer metastatic behavior by microRNAs targeting EMT transcription factors. A relevant participation of miR-196a-5p and miR-22-3p in ZEB1 expression.Breast cancer research and treatment · 2025Article
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- Transparent 3-Layered Bacterial Nanocellulose as a Multicompartment and Biomimetic Scaffold for Co-Culturing Cells.Journal of functional biomaterials · 2025Article
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- The Application of Dendritic Cells Vaccines in Tumor Therapy and Their Combination with Biomimetic Nanoparticles.Vaccines · 2025Review
- Anti-metastasis Effects and Mechanism of Action of Curcumin Analog (2E,6E)-2,6-bis(2,3-dimethoxybenzylidene) Cyclohexanone (DMCH) on the SW620 Colorectal Cancer Cell Line.Anti-cancer agents in medicinal chemistry · 2025Article
- SpottedPy quantifies relationships between spatial transcriptomic hotspots and uncovers environmental cues of epithelial-mesenchymal plasticity in breast cancer.Genome biology · 2024Article
- NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid.BMC cancer · 2024Article
- Transcriptional responses to direct and indirect TGFB1 stimulation in cancerous and noncancerous mammary epithelial cells.Cell communication and signaling : CCS · 2024Article
- Article
- Brain endothelial cells promote breast cancer cell extravasation to the brain via EGFR-DOCK4-RAC1 signalling.Communications biology · 2024Article
119 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells frequently disseminate through the lymphatic system during metastatic spread of breast cancer and many other types of cancer. Yet it is not clear how tumor cells make their way into the lymphatic system and how they choose between lymphatic and blood vessels for migration. Here we report that mammary tumor cells undergoing epithelial-mesenchymal transition (EMT) in response to transforming growth factor-β (TGF-β1) become activated for targeted migration through the lymphatic system, similar to dendritic cells (DCs) during inflammation. EMT cells preferentially migrated toward lymphatic vessels compared with blood vessels, both in vivo and in 3D cultures. A mechanism of this targeted migration was traced to the capacity of TGF-β1 to promote CCR7/CCL21-mediated crosstalk between tumor cells and lymphatic endothelial cells. On one hand, TGF-β1 promoted CCR7 expression in EMT cells through p38 MAP kinase-mediated activation of the JunB transcription factor. Blockade of CCR7, or treatment with a p38 MAP kinase inhibitor, reduced lymphatic dissemination of EMT cells in syngeneic mice. On the other hand, TGF-β1 promoted CCL21 expression in lymphatic endothelial cells. CCL21 acted in a paracrine fashion to mediate chemotactic migration of EMT cells toward lymphatic endothelial cells. The results identify TGF-β1-induced EMT as a mechanism, which activates tumor cells for targeted, DC-like migration through the lymphatic system. Furthermore, it suggests that p38 MAP kinase inhibition may be a useful strategy to inhibit EMT and lymphogenic spread of tumor cells.
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