ArticleMolecular oncology2020
Estrogen receptor α promotes lung cancer cell invasion via increase of and cross-talk with infiltrated macrophages through the CCL2/CCR2/MMP9 and CXCL12/CXCR4 signaling pathways.
Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Diagnostic Value of CCL2 and CCR2 in Pleural Effusion for Distinguishing Lung Cancer Histological Subtypes: A Retrospective Study.Diagnostic cytopathology · 2026Article
- Gender disparities in the overall survival of patients with minimally invasive squamous cell carcinoma of the lung: a retrospective analysis of the Surveillance, Epidemiology, and End Results Program database.Translational lung cancer research · 2026Article
- Understanding the dual role of granulocyte-macrophage colony-stimulating factor in the lung cancer tumor microenvironment and its therapeutic implications.Translational lung cancer research · 2026Review
- CRISPR activation screens identify oncogenic lncRNAs that are susceptible to CDK4/6 inhibitor treatment.Nature communications · 2026Article
- Encoding functional edges in graphs to model spatially varying relationships in the tumor microenvironment.NPJ artificial intelligence · 2026Article
- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- Review
- Lung cancer in non-smoking women (LCINSW): from risk factors to precision therapy.Cancer metastasis reviews · 2025Review
- Prognostic influence of chronic inflammation in patients with head and neck cancer based on sex differences.Clinical & experimental metastasis · 2025Review
- The Mechanism of Steroid Hormones in Non-Small Cell Lung Cancer: From Molecular Signaling to Clinical Application.Biomedicines · 2025Review
- Nanoparticle-Mediated CXCL12-CXCR4 Inhibition Reprograms Macrophages and Suppresses Gastric Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ERα-dependent crosstalk between macrophages and cancer cells potentiates vasculogenic mimicry and M2 macrophage polarization in bladder cancer.Cell communication and signaling : CCS · 2025Article
- Estrogen receptor α suppresses hepatocellular carcinoma by restricting M2 macrophage infiltration through the YAP-CCL2 axis.BMC cancer · 2025Article
- Transcription factors and hormone receptors: Sex‑specific targets for cancer therapy (Review).Oncology letters · 2025Review
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Senescence-associated secretory phenotype in lung cancer: remodeling the tumor microenvironment for metastasis and immune suppression.Frontiers in oncology · 2025Review
- Expression patterns of estrogen and androgen receptors in NSCLC patients according to the PD-L1 profile.Frontiers in immunology · 2025Article
- Sex hormones and immune regulation in ovarian cancer.Discover oncology · 2024Review
- Network Pharmacology and Molecular Docking Study on the Mechanism of the Therapeutic Effect of Strychni Semen in NSCLC.Biological procedures online · 2024Article
- The immune cells causative role in lung cancer: Mendelian randomization study.Discover oncology · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Data analysis of clinical samples suggests that higher estrogen receptor α (ERα) expression could be associated with worse overall survival in some patients with non-small-cell lung cancer (NSCLC). Immunofluorescence results further showed that higher ERα expression was linked to larger numbers of infiltrated macrophages in NSCLC tissues. However, the detailed mechanisms underlying this phenomenon remain unclear. Results from in vitro studies with multiple cell lines revealed that, in NSCLC cells, ERα can activate the CCL2/CCR2 axis to promote macrophage infiltration, M2 polarization, and MMP9 production, which can then increase NSCLC cell invasion. Mechanistic studies using chromatin immunoprecipitation and promoter luciferase assays demonstrated that ERα could bind to estrogen response elements (EREs) on the CCL2 promoter to increase CCL2 expression. Furthermore, ERα-increased macrophage infiltration can induce a positive feedback mechanism to increase lung cancer cell ERα expression via the up-regulation of the CXCL12/CXCR4 pathway. Targeting these newly identified pathways, NSCLC ERα-increased macrophage infiltration or the macrophage-to-NSCLC CXCL12/CXCR4/ERα signal, with anti-estrogens or CCR2/CXCR4 antagonists, may help in the development of new alternative therapies to better treat NSCLC.
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Registered trials
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.