ArticleThe Journal of biological chemistry2012
Estrogen represses hepatocellular carcinoma (HCC) growth via inhibiting alternative activation of tumor-associated macrophages (TAMs).
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.
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Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Molecular mechanisms of sex hormones in Hepatocellular Carcinoma: a systematic review.Molecular biology reports · 2025Pooled it
- Intricate roles of estrogen and estrogen receptors in digestive system cancers: a systematic review.Cancer biology & medicine · 2024Pooled it
- M2-associated microglial states in oligodendrocyte regulation and white matter repair in vascular dementia.Journal of translational medicine · 2026Review
- Sex of central neurons controls intestinal niche signalling to drive sex differences in stem cell activity and cancer susceptibility.Nature communications · 2026Article
- Intratumoral but not circulating estradiol predicts postoperative survival in men with hepatocellular carcinoma.Discover oncology · 2026Article
- Estrogen Promotes Melanogenesis Through Facilitating M2 Macrophage Skewing in Melasma.International journal of molecular sciences · 2026Article
- Age modulates estradiol's dual role in hepatocellular carcinoma recurrence after ablation: A prospective observational study.iScience · 2026Article
- The role of iron in driving sex-biased differences in cancer.Cancer metastasis reviews · 2026Review
- Sex based relative expression of estrogen receptors and tumor necrosis factor-alpha in liver affects hepatitis C virus viral pathogenesis.World journal of gastroenterology · 2025Article
- Epidemiological and demographic analysis of liver cancer attributable to modifiable risk factors from 1990 to 2021.Scientific reports · 2025Article
- The Role of Heavy Metals in the Biology of Female Cancers.International journal of molecular sciences · 2025Review
- Exosome-based immunotherapy in hepatocellular carcinoma.Clinical and experimental medicine · 2025Review
- Transcription factors and hormone receptors: Sex‑specific targets for cancer therapy (Review).Oncology letters · 2025Review
- Estrogen and viral infection.Frontiers in immunology · 2025Review
- Modulation of STAT6 signaling for hepatoprotection.Frontiers in pharmacology · 2025Review
- Sex disparities in hepatocellular carcinoma immunotherapy: hormonal and genetic influences on treatment efficacy.Frontiers in immunology · 2025Review
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Gamma-tocotrienol Inhibits Proliferation and Growth of HSD17B4 Overexpressing HepG2 Liver Cancer Cells.Current cancer drug targets · 2025Article
- The Influence of ESR2 Gene Polymorphisms on Susceptibility to Hepatitis B Virus-Related Chronic Hepatitis, Liver Cirrhosis, and Hepatocellular Carcinoma.Biochemical genetics · 2024Article
- Sex difference in human diseases: mechanistic insights and clinical implications.Signal transduction and targeted therapy · 2024Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocarcinoma cancer (HCC) occurs more often in men than in women, and little is known about its underlying molecular mechanisms.
resultsWe identify that 17β-estradiol (E2) could suppress tumor growth via regulating the polarization of macrophages.
conclusionEstrogen functions as a suppressor for macrophage alternative activation. SIGNIFICANCE: These studies introduce a novel mechanism for suppressing male-predominant HCC. Hepatocarcinoma cancer (HCC), one of the most malignant cancers, occurs significantly more often in men than in women; however, little is known about its underlying molecular mechanisms. Here we identified that 17β-estradiol (E2) could suppress tumor growth via regulating the polarization of macrophages. We showed that E2 re-administration reduced tumor growth in orthotopic and ectopic mice HCC models. E2 functioned as a suppressor for macrophage alternative activation and tumor progression by keeping estrogen receptor β (ERβ) away from interacting with ATP5J (also known as ATPase-coupling factor 6), a part of ATPase, thus inhibiting the JAK1-STAT6 signaling pathway. These studies introduce a novel mechanism for suppressing male-predominant HCC.
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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.