ArticleMolecular cancer2019
MCT-1/miR-34a/IL-6/IL-6R signaling axis promotes EMT progression, cancer stemness and M2 macrophage polarization in triple-negative breast cancer.
Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 3 of them syntheses that pooled it.
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Who cites it
297 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Unraveling Biomarker Signatures in Triple-Negative Breast Cancer: A Systematic Review for Targeted Approaches.International journal of molecular sciences · 2024Pooled it
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- A comprehensive analysis of the role of QPRT in breast cancer.Scientific reports · 2023Pooled it
- Effects of ultrasound-guided nerve block combined with PCIA analgesia on postoperative pain, inflammatory response, hospital stay, and adverse reactions in breast cancer surgery.African health sciences · 2025Trial
- Tumor-educated macrophages promote cytokine-driven lung colonization in triple-negative breast cancer.Oncoimmunology · 2026Article
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- Myeloid-derived suppressor cells in cancer: biology, regulatory networks and theranostic prospects.Signal transduction and targeted therapy · 2026Review
- Chiral Titanium Dioxide Nanoparticles Induce Breast Cancer Lung Metastasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Spatial organization of the TNBC tumor microenvironment: multicellular niches, T-cell bottlenecks, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Engineering the tumor immune landscape: Translating non-invasive physical stimulation into tumor-associated macrophage-targeted cancer immunotherapy.Bioengineering & translational medicine · 2026Review
- A prediction model for targeted drug resistance in renal cell carcinoma based on plasma proteomics analysis.Translational andrology and urology · 2026Article
- Beyond a waste product: lactate as a master metabolite dictating anti-tumor T-cell fate.Cell death & disease · 2026Review
- ESM1 drives cisplatin resistance and ferroptosis resistance via ERBB2/FAK/SRC/HSPB1/NF-κB signaling in ovarian cancer.iScience · 2026Article
- Identification of Candidate mRNA and miRNA Molecules Associated with Tuberculosis Through Preliminary Analysis and Validation Using Clinical Samples.International journal of molecular sciences · 2026Article
- Efficacy and safety of tocilizumab for neoplastic fever in patients with advanced solid tumors: a multicenter retrospective study.The oncologist · 2026Article
- Epithelial-mesenchymal transition and immunosuppression: Two sides of the same coin.Cellular and molecular life sciences : CMLS · 2026Review
- Hesperetin-black phosphorus nanosheets targeting TAMs induce ferroptosis and reverse protumoral polarization to remodel the immune microenvironment.Materials today. Bio · 2026Article
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- Research progress and trends on M2 macrophages in breast cancer research: a bibliometric analysis.Discover oncology · 2026Article
237 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
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Abstract
backgroundTriple-negative breast cancer (TNBC) is a poor prognostic breast cancer with the highest mutations and limited therapeutic choices. Cytokine networking between cancer cells and the tumor microenvironment (TME) maintains the self-renewing subpopulation of breast cancer stem cells (BCSCs) that mediate tumor heterogeneity, resistance and recurrence. Immunotherapy of those factors combined with targeted therapy or chemoagents may advantage TNBC treatment.
resultsWe found that the oncogene Multiple Copies in T-cell Malignancy 1 (MCT-1/MCTS1) expression is a new poor-prognosis marker in patients with aggressive breast cancers. Overexpressing MCT-1 perturbed the oncogenic breast epithelial acini morphogenesis and stimulated epithelial-mesenchymal transition and matrix metalloproteinase activation in invasive TNBC cells, which were repressed after MCT-1 gene silencing. As mammary tumor progression was promoted by oncogenic MCT-1 activation, tumor-promoting M2 macrophages were enriched in TME, whereas M2 macrophages were decreased and tumor-suppressive M1 macrophages were increased as the tumor was repressed via MCT-1 knockdown. MCT-1 stimulated interleukin-6 (IL-6) secretion that promoted monocytic THP-1 polarization into M2-like macrophages to increase TNBC cell invasiveness. In addition, MCT-1 elevated the soluble IL-6 receptor levels, and thus, IL-6R antibodies antagonized the effect of MCT-1 on promoting M2-like polarization and cancer cell invasion. Notably, MCT-1 increased the features of BCSCs, which were further advanced by IL-6 but prevented by tocilizumab, a humanized IL-6R antibody, thus MCT-1 knockdown and tocilizumab synergistically inhibited TNBC stemness. Tumor suppressor miR-34a was induced upon MCT-1 knockdown that inhibited IL-6R expression and activated M1 polarization.
conclusionsThe MCT-1 pathway is a novel and promising therapeutic target for TNBC.
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