ArticleCancer biology & therapy2020
Cytokines secreted by stromal cells in TNBC microenvironment as potential targets for cancer therapy.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Unraveling Biomarker Signatures in Triple-Negative Breast Cancer: A Systematic Review for Targeted Approaches.International journal of molecular sciences · 2024Pooled it
- Exosomal EPHA2 transfers metastatic potential by stabilizing TGF-βRI and activating the TGF-β/SMAD3 signaling pathway in breast cancer.Cancer biology & medicine · 2026Article
- Construction of circadian clock signature for tumor microenvironment in predicting survival of esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- Advancements in research regarding the influence of the tumor microenvironment on the proliferation and metastasis of osteosarcoma (Review).Oncology letters · 2026Review
- Lipocalin-2 in Triple-Negative Breast Cancer: A Review of Its Pathophysiological Role in the Metastatic Cascade.International journal of molecular sciences · 2025Review
- Application of Gene Editing Technology Based on Targeted Delivery Materials in TNBC.ACS omega · 2025Review
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- EGFRvIII-driven microenvironmental fibroblast activation and transformation accelerate oral cancer progression via lipocalin-2/STAT3 axis.Neoplasia (New York, N.Y.) · 2025Article
- Biomarkers of mRNA vaccine efficacy derived from mechanistic modeling of tumor-immune interactions.PLoS computational biology · 2025Article
- Cancer-Derived Extracellular Vesicle ITGB2 Promotes the Progression of Triple-Negative Breast Cancer via the Activation of Cancer-Associated Fibroblasts.Global challenges (Hoboken, NJ) · 2025Article
- Inflammation-associated drug resistance and tumor growth in TNBC.Frontiers in immunology · 2025Review
- Tumor microenvironment and immunotherapy for triple-negative breast cancer.Biomarker research · 2024Review
- Associations between plasma markers and symptoms of anxiety and depression in patients with breast cancer.BMC psychiatry · 2024Article
- WTAP Mediates NUPR1 Regulation of LCN2 Through mBiochemical genetics · 2024Article
- Truncated O-glycosylation in metastatic triple-negative breast cancer reveals a gene expression signature associated with extracellular matrix and proteolysis.Scientific reports · 2024Article
- Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Lipocalin-2 promotes breast cancer brain metastasis by enhancing tumor invasion and modulating brain microenvironment.Frontiers in oncology · 2024Review
- Lipocalin-2: A Nurturer of Tumor Progression and a Novel Candidate for Targeted Cancer Therapy.Cancers · 2023Review
- A transcriptome-informed QSP model of metastatic triple-negative breast cancer identifies predictive biomarkers for PD-1 inhibition.Science advances · 2023Article
- The role and regulation of Maf proteins in cancer.Biomarker research · 2023Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
In triple-negative breast cancer (TNBC), the lack of therapeutic markers and effective targeted therapies result in an incurable metastatic disease associated with a poor prognosis. Crosstalks within the tumor microenvironment (TME), including those between cancer and stromal cells, affect the tumor heterogeneity, growth, and metastasis. Previously, we have demonstrated that IL-6, IL-8, and CCL5 play a significant role in TNBC growth and metastasis. In this study, we performed a systematic analysis of cytokine factors secreted from four stromal components (fibroblasts, macrophages, lymphatic endothelial cells, and blood microvascular endothelial cells) induced by four TNBC cell types. Through bioinformatic analysis, we selected putative candidates of secreted factors from stromal cells, which are involved in EMT activity, cell proliferation, metabolism, and matrisome pathways. Among the candidates, LCN2, GM-CSF, CST3, IL-6, IL-8, and CHI3L1 are ranked highly. Significantly, Lipocalin-2 (LCN2) is upregulated in the crosstalk of stromal cells and four different TNBC cells. We validated the increase of LCN2 secreted from four stromal cells induced by TNBC cells. Using a specific LCN2 antibody, we observed the inhibition of TNBC cell growth and migration. Taken together, these results propose secreted factors as molecular targets to treat TNBC progression via crosstalk with stromal components.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.