ArticleiScience2024
Androgen receptor-induced molecules and androgen contribute synergistically to male-predominance of hepatocellular carcinoma.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Androgen receptor drives lenvatinib resistance in hepatocellular carcinoma through transcriptional activation of EIF3I and a downstream ceRNA axis.Oncology letters · 2026Article
- Functional cure for chronic hepatitis B on hepatocellular carcinoma prevention: Evidence and clinical implications.iLIVER · 2026Review
- Insulin-like growth factor binding protein-3 serves as a biomarker for resistance to enzalutamide in prostate cancer.Apoptosis : an international journal on programmed cell death · 2026Article
- Occult hepatitis B virus infection among hepatitis B surface antigen negative vaccinated healthcare workers in East Gojjam zone hospitals.Scientific reports · 2026Article
- Radiographic evidence of thymic involution in hepatocellular carcinoma: a propensity score-matched study in viral cirrhosis.Frontiers in immunology · 2026Article
- Testosterone and Androgen Receptor in Cancers with Significant Sex Dimorphism in Incidence Rates and Survival.Cancers · 2025Review
- Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to clarify the mechanisms of male predominance of hepatitis B virus (HBV) -related hepatocellular carcinoma (HCC). Androgen receptor (AR) facilitates HCC cell growth, which was augmented by androgen (dihydrotestosterone [DHT]) and attenuated by anti-androgen (flutamide). AR upregulated the expressions of BIRC7, IGFBP3, and NTSR1 via increasing their promoter activities, which were enhanced by DHT. Wild-type HBV X (WT-HBx) upregulated AR transcription, which depended on DHT; whereas the effect of C-terminal carboxy-truncated HBx on AR transcription was independent of DHT. BIRC7, IGFBP3, and NTSR1 increased the growth of HCC. High expression of BIRC7 and NTSR1 contributes to poor HCC outcomes in male patients, but not in female patients. Downregulation of NTSR1 inhibits tumor growth in male mice rather than in female mice. Conclusively, AR promotes HCC at least partially via upregulating BIRC7, IGFBP3, and NTSR1, which is enhanced by androgen and HBx. BIRC7 and NTSR1 facilitate HCC progression in a male-predominant manner.
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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.