ArticleCells2020
Paracrine Signaling from Breast Cancer Cells Causes Activation of ID4 Expression in Tumor-Associated Macrophages.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Paclitaxel drives TREM2Nature communications · 2026Article
- The Critical Role of Inhibitor of Differentiation 4 in Breast Cancer: From Mammary Gland Development to Tumor Progression.Cancer medicine · 2025Review
- Assessment of ID family proteins expression in colorectal cancer of Iraqi patients.Molecular biology reports · 2024Article
- Ensemble learning model for identifying the hallmark genes of NFκB/TNF signaling pathway in cancers.Journal of translational medicine · 2023Article
- MALAT1-dependent hsa_circ_0076611 regulates translation rate in triple-negative breast cancer.Communications biology · 2022Article
- Non-Coding RNAs in the Crosstalk between Breast Cancer Cells and Tumor-Associated Macrophages.Non-coding RNA · 2022Review
- Upregulated circTMEM59 Inhibits Cell Growth and Metastasis by miR-668-3p/ID4 Axis in Colorectal Cancer.Oxidative medicine and cellular longevity · 2022Article
- Tumor-Associated Macrophages: Key Players in Triple-Negative Breast Cancer.Frontiers in oncology · 2022Review
- Review
- Tumor Microenvironment: Key Players in Triple Negative Breast Cancer Immunomodulation.Cancers · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor-associated macrophages (TAMs) constitute a major portion of the leukocyte infiltrate found in breast cancer (BC). BC cells may reprogram TAMs in a pro-angiogenic and immunosuppressive sense. We previously showed that high expression of the ID4 protein in triple-negative BC cells leads to the induction of a proangiogenic program in TAMs also through the downregulation of miR-107. Here, we investigated the expression and function of the ID4 protein in TAMs.
methodsHuman macrophages obtained from peripheral blood-derived monocytes (PBDM) and mouse RAW264.7 cells were used as macrophage experimental systems. ID4-correlated mRNAs of the TCGA and E-GEOD-18295 datasets were analyzed.
resultsWe observed that BC cells determine a paracrine induction of ID4 expression and activation of the ID4 promoter in neighboring macrophages. Interestingly, ID4 expression is higher in macrophages associated with invasive tumor cells compared to general TAMs, and ID4-correlated mRNAs are involved in various pathways that were previously reported as relevant for TAM functions. Selective depletion of ID4 expression in macrophages enabled validation of the ability of ID4 to control the expression of YAP1 and of its downstream targets CTGF and CYR61.
conclusionCollectively, our results show that activation of ID4 expression in TAMs is observed as a consequence of BC cell paracrine activity and could participate in macrophage reprogramming in BC.
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