ArticleBreast cancer research : BCR2017
Pathomimetic avatars reveal divergent roles of microenvironment in invasive transition of ductal carcinoma in situ.
Article in Breast cancer research : BCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Article
- Review
- Models for Studying Ductal Carcinoma In Situ Progression.Advances in experimental medicine and biology · 2025Review
- Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance.Signal transduction and targeted therapy · 2024Review
- Establishment of a 3D co-culture model to investigate the role of primary fibroblasts in ductal carcinoma in situ of the breast.Cancer reports (Hoboken, N.J.) · 2023Article
- Identification of key pathways and genes in vestibular schwannoma using bioinformatics analysis.Experimental and therapeutic medicine · 2022Article
- Ductal Carcinoma in Situ: Molecular Changes Accompanying Disease Progression.Journal of mammary gland biology and neoplasia · 2022Review
- Modeling Tumor: Lymphatic Interactions in Lymphatic Metastasis of Triple Negative Breast Cancer.Cancers · 2021Article
- Review
- Cancer Cell Invasion of Mammary Organoids with Basal-In Phenotype.Advanced healthcare materials · 2021Article
- Sharp Downregulation of Hub Genes Associated With the Pathogenesis of Breast Cancer From Ductal CarcinomaFrontiers in oncology · 2021Article
- Loss of myoepithelial calponin-1 characterizes high-risk ductal carcinoma in situ cases, which are further stratified by T cell composition.Molecular carcinogenesis · 2020Article
- Gene Editing of α6 Integrin Inhibits Muscle Invasive Networks and Increases Cell-Cell Biophysical Properties in Prostate Cancer.Cancer research · 2019Article
- Spatio-temporal modeling and live-cell imaging of proteolysis in the 4D microenvironment of breast cancer.Cancer metastasis reviews · 2019Review
- In Vitro Models for Studying Invasive Transitions of Ductal Carcinoma In Situ.Journal of mammary gland biology and neoplasia · 2019Review
- Intratumoral Heterogeneity in Ductal Carcinoma In Situ: Chaos and Consequence.Journal of mammary gland biology and neoplasia · 2018Review
- Breaking through to the Other Side: Microenvironment Contributions to DCIS Initiation and Progression.Journal of mammary gland biology and neoplasia · 2018Review
- Downregulation of Rap1Gap: A Switch from DCIS to Invasive Breast Carcinoma via ERK/MAPK Activation.Neoplasia (New York, N.Y.) · 2018Article
- IL-6-mediated cross-talk between human preadipocytes and ductal carcinoma in situ in breast cancer progression.Journal of experimental & clinical cancer research : CR · 2018Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe breast tumor microenvironment regulates progression of ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC). However, it is unclear how interactions between breast epithelial and stromal cells can drive this progression and whether there are reliable microenvironmental biomarkers to predict transition of DCIS to IDC.
methodsWe used xenograft mouse models and a 3D pathomimetic model termed mammary architecture and microenvironment engineering (MAME) to study the interplay between human breast myoepithelial cells (MEPs) and cancer-associated fibroblasts (CAFs) on DCIS progression.
resultsOur results show that MEPs suppress tumor formation by DCIS cells in vivo even in the presence of CAFs. In the in vitro MAME model, MEPs reduce the size of 3D DCIS structures and their degradation of extracellular matrix. We further show that the tumor-suppressive effects of MEPs on DCIS are linked to inhibition of urokinase plasminogen activator (uPA)/urokinase plasminogen activator receptor (uPAR)-mediated proteolysis by plasminogen activator inhibitor 1 (PAI-1) and that they can lessen the tumor-promoting effects of CAFs by attenuating interleukin 6 (IL-6) signaling pathways.
conclusionsOur studies using MAME are, to our knowledge, the first to demonstrate a divergent interplay between MEPs and CAFs within the DCIS tumor microenvironment. We show that the tumor-suppressive actions of MEPs are mediated by PAI-1, uPA and its receptor, uPAR, and are sustained even in the presence of the CAFs, which themselves enhance DCIS tumorigenesis via IL-6 signaling. Identifying tumor microenvironmental regulators of DCIS progression will be critical for defining a robust and predictive molecular signature for clinical use.
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