ArticleFrontiers in immunology2024
GPER1 signaling restricts macrophage proliferation and accumulation in human hepatocellular carcinoma.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Immune-related biomarkers for major depressive disorder identified via integrated bioinformatics and machine learning.European journal of psychotraumatology · 2026Review
- Molecular mechanisms and clinical impacts of sex differences in urologic cancers.Discover oncology · 2026Review
- Molecular mechanisms of tumor-associated macrophages in hepatocellular carcinoma development and therapy.World journal of gastroenterology · 2026Review
- Sex disparities in hepatocellular carcinoma immunotherapy: hormonal and genetic influences on treatment efficacy.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
Funding
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Abstract
Background: Sex hormones and their related receptors have been reported to impact the development and progression of tumors. However, their influence on the composition and function of the tumor microenvironment is not well understood. We aimed to investigate the influence of sex disparities on the proliferation and accumulation of macrophages, one of the major components of the tumor microenvironment, in hepatocellular carcinoma (HCC). Methods: Immunohistochemistry was applied to assess the density of immune cells in HCC tissues. The role of sex hormone related signaling in macrophage proliferation was determined by immunofluorescence and flow cytometry. The underlying regulatory mechanisms were examined with both Results: We found higher levels of macrophage proliferation and density in tumor tissues from male patients compared to females. The expression of G protein-coupled estrogen receptor 1 (GPER1), a non-classical estrogen receptor, was significantly decreased in proliferating macrophages, and was inversely correlated with macrophage proliferation in HCC tumors. Activation of GPER1 signaling with a selective agonist G-1 suppressed macrophage proliferation by downregulating the MEK/ERK pathway. Additionally, G-1 treatment reduced PD-L1 expression on macrophages and delayed tumor growth in mice. Moreover, patients with a higher percentage of GPER1 Conclusions: These findings reveal a novel role of GPER1 signaling in regulating macrophage proliferation and function in HCC tumors and may offer a potential strategy for designing therapies based on understanding sex-related disparities of patients.
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