ArticleFrontiers in oncology2015
TGF-β1-Induced Epithelial-Mesenchymal Transition Promotes Monocyte/Macrophage Properties in Breast Cancer Cells.
Article in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- LMO2 Regulates Epithelial-Mesenchymal Plasticity of Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2026Article
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.Cancer cell international · 2025Review
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- Gemcitabine combination therapies induce apoptosis in uterine carcinosarcoma patient-derived organoids.Frontiers in oncology · 2024Article
- TGFß1 Stimulates Lymphatic Endothelial Cells to Produce IL7 and IL15, Which Act as Chemotactic Factors for Breast Cancer Cells with Mesenchymal Properties.Journal of mammary gland biology and neoplasia · 2023Article
- The RELT Family of Proteins: An Increasing Awareness of Their Importance for Cancer, the Immune System, and Development.Biomedicines · 2023Review
- Evaluation of ITGB1 expression as a predictor of the therapeutic effects of immune checkpoint inhibitors in gastric cancer.BMC gastroenterology · 2023Article
- The ELF3 transcription factor is associated with an epithelial phenotype and represses epithelial-mesenchymal transition.Journal of biological engineering · 2023Article
- Identification and validation of EMT-immune-related prognostic biomarkers CDKN2A, CMTM8 and ILK in colon cancer.BMC gastroenterology · 2022Article
- KLF4 Induces Mesenchymal-Epithelial Transition (MET) by Suppressing Multiple EMT-Inducing Transcription Factors.Cancers · 2021Article
- miR‑29b suppresses proliferation and induces apoptosis of hepatocellular carcinoma ascites H22 cells via regulating TGF‑β1 and p53 signaling pathway.International journal of molecular medicine · 2021Article
- RELT promotes the growth of esophageal squamous cell carcinoma by activating the NF-κB pathway.Cell cycle (Georgetown, Tex.) · 2021Article
- Polyphenols Modulating Effects of PD-L1/PD-1 Checkpoint and EMT-Mediated PD-L1 Overexpression in Breast Cancer.Nutrients · 2021Review
- Evaluation of circulating microRNAs-211 and 25 as diagnostic biomarkers of colorectal cancer.Molecular biology reports · 2021Article
- Calcium Channel Protein ORAI1 Mediates TGF-β Induced Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- CRISPR/Cas9 based genome editing for targeted transcriptional control in triple-negative breast cancer.Computational and structural biotechnology journal · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer progression toward metastatic disease is linked to re-activation of epithelial-mesenchymal transition (EMT), a latent developmental process. Breast cancer cells undergoing EMT lose epithelial characteristics and gain the capacity to invade the surrounding tissue and migrate away from the primary tumor. However, less is known about the possible role of EMT in providing cancer cells with properties that allow them to traffic to distant sites. Given the fact that pro-metastatic cancer cells share a unique capacity with immune cells to traffic in-and-out of blood and lymphatic vessels we hypothesized that tumor cells undergoing EMT may acquire properties of immune cells. To study this, we performed gene-profiling analysis of mouse mammary EpRas tumor cells that had been allowed to adopt an EMT program after long-term treatment with TGF-β1 for 2 weeks. As expected, EMT cells acquired traits of mesenchymal cell differentiation and migration. However, in addition, we found another cluster of induced genes, which was specifically enriched in monocyte-derived macrophages, mast cells, and myeloid dendritic cells, but less in other types of immune cells. Further studies revealed that this monocyte/macrophage gene cluster was enriched in human breast cancer cell lines displaying an EMT or a Basal B profile, and in human breast tumors with EMT and undifferentiated (ER-/PR-) characteristics. The results identify an EMT-induced monocyte/macrophage gene cluster, which may play a role in breast cancer cell dissemination and metastasis.
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