ArticleMolecular oncology2018
Basal-like breast cancer engages tumor-supportive macrophages via secreted factors induced by extracellular S100A4.
Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 39 citations in OpenAlex.
- Extracellular adenosine triphosphate upregulates S100A4 expression and promotes the migration and invasion of breast cancer cells via P2Y2/SOX9 signaling.Translational cancer research · 2026Article
- S100A4-TLR4-TGF-β axis as a therapeutic target for Dupuytren's contracture in diabetic patients.Cell death discovery · 2026Article
- Colostrum extracellular vesicles are neuroprotective in models of Parkinson's disease.Theranostics · 2026Article
- Tumor Microenvironment On-A-Chip and Single-Cell Analysis Reveal Synergistic Stromal-Immune Crosstalk on Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integration of scRNA-seq and bulk RNA-seq to reveal the association and potential molecular mechanisms of metabolic reprogramming regulated by lactylation and chemotherapy resistance in ovarian cancer.Frontiers in immunology · 2025Article
- Pilot study: Initial investigation suggests differences in EMT-associated gene expression in breast tumor regions.Computational and structural biotechnology journal · 2025Article
- The multi-faceted immune modulatory role of S100A4 in cancer and chronic inflammatory disease.Frontiers in immunology · 2025Review
- Role of indoleamine 2, 3-dioxygenase 1 in immunosuppression of breast cancer.Cancer pathogenesis and therapy · 2024Review
- ANXA9 facilitates S100A4 and promotes breast cancer progression through modulating STAT3 pathway.Cell death & disease · 2024Article
- Novel mechanism of drug resistance triggered by tumor-associated macrophages through Heat Shock Factor-1 activation.Cancer immunology, immunotherapy : CII · 2024Article
- RAGE and its ligands in breast cancer progression and metastasis.Oncology reviews · 2024Review
- The cellular composition of the tumor microenvironment is an important marker for predicting therapeutic efficacy in breast cancer.Frontiers in immunology · 2024Review
- Deconvolution of cancer cell states by the XDec-SM method.PLoS computational biology · 2023Article
- Polyploid giant cancer cells, cytokines and cytomegalovirus in breast cancer progression.Cancer cell international · 2023Article
- Metabolic Reprogramming of Breast Tumor-Educated Macrophages Revealed by NMR Metabolomics.Cancers · 2023Article
- Regulation of Inflammasome by microRNAs in Triple-Negative Breast Cancer: New Opportunities for Therapy.International journal of molecular sciences · 2023Review
- Comparative analysis of clinicopathological characteristics of central necrotizing breast cancer and basal cell-like breast cancer.Frontiers in oncology · 2023Article
- Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway.Cell adhesion & migration · 2022Article
- Epithelial Mesenchymal Transition and Immune Response in Metaplastic Breast Carcinoma.International journal of molecular sciences · 2021Review
- Tumor Microenvironment: Key Players in Triple Negative Breast Cancer Immunomodulation.Cancers · 2021Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor microenvironment (TME) may influence both cancer progression and therapeutic response. In breast cancer, particularly in the aggressive triple-negative/basal-like subgroup, patient outcome is strongly associated with the tumor's inflammatory profile. Tumor-associated macrophages (TAMs) are among the most abundant immune cells in the TME, shown to be linked to poor prognosis and therapeutic resistance. In this study, we investigated the effect of the metastasis- and inflammation-associated microenvironmental factor S100A4 on breast cancer cells (BCCs) of different subtypes and explored their further interactions with myeloid cells. We demonstrated that extracellular S100A4 activates BCCs, particularly the basal-like subtype, to elevate secretion of pro-inflammatory cytokines. The secreted factors promoted conversion of monocytes to TAM-like cells that exhibited protumorigenic activities: stimulated epithelial-mesenchymal transition, proliferation, chemoresistance, and motility in cancer cells. In conclusion, we have shown that extracellular S100A4 instigates a tumor-supportive microenvironment, involving a network of cytokines and TAM-like cells, which was particularly characteristic for basal-like BCCs and potentiated their aggressive properties. The S100A4-BCC-TAM interaction cascade could be an important contributor to the aggressive behavior of this subtype and should be further explored for therapeutic targeting.
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