ArticleOncology research2019
E2-Induced Activation of the NLRP3 Inflammasome Triggers Pyroptosis and Inhibits Autophagy in HCC Cells.
Article in Oncology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 208 citations in OpenAlex.
- Review
- Age modulates estradiol's dual role in hepatocellular carcinoma recurrence after ablation: A prospective observational study.iScience · 2026Article
- Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway.International dental journal · 2026Article
- Therapeutic effects of Tuolitounong decoction on pyroptosis in granulomatous lobular mastitis: evidence from in vitro and in vivo models.Journal of molecular histology · 2026Article
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
- Curcumin as a Dual Modulator of Pyroptosis: Mechanistic Insights and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Schisandrin C Improves Chronic Stress-Induced Dyslipidemia in Mice by Regulating Pyroptosis and Autophagy Levels.Journal of microbiology and biotechnology · 2025Article
- Unveiling the nexus: pyroptosis and its crucial implications in liver diseases.Molecular and cellular biochemistry · 2025Review
- The Role of the Tumor Microenvironment (TME) in Advancing Cancer Therapies: Immune System Interactions, Tumor-Infiltrating Lymphocytes (TILs), and the Role of Exosomes and Inflammasomes.International journal of molecular sciences · 2025Review
- Platelet-rich plasma combined with isometric quadriceps contraction regulates autophagy in chondrocytes via the PI3K/AKT/mTOR pathway to promote cartilage repair in knee osteoarthritis.Regenerative therapy · 2025Article
- Mitochondrial alterations and signatures in hepatocellular carcinoma.Cancer metastasis reviews · 2025Review
- Molecular characteristics, clinical significance and cancer‑immune interactions of pyroptosis‑related genes in colorectal cancer.Oncology letters · 2025Article
- Dual role of pyroptosis in liver diseases: mechanisms, implications, and therapeutic perspectives.Frontiers in cell and developmental biology · 2025Review
- Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.Molecular medicine (Cambridge, Mass.) · 2024Review
- Crosstalk of pyroptosis and cytokine in the tumor microenvironment: from mechanisms to clinical implication.Molecular cancer · 2024Review
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- The role of pyroptosis in cancer: key components and therapeutic potential.Cell communication and signaling : CCS · 2024Review
- Sex difference in human diseases: mechanistic insights and clinical implications.Signal transduction and targeted therapy · 2024Review
- Ferroptosis, pyroptosis and necroptosis in hepatocellular carcinoma immunotherapy: Mechanisms and immunologic landscape (Review).International journal of oncology · 2024Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence suggests that 17β-estradiol (E2) and estrogen receptor (ER) signaling are protective against hepatocellular carcinoma (HCC). In our previous study, we showed that E2 suppressed the carcinogenesis and progression of HCC by targeting NLRP3 inflammasome activation, whereas the molecular mechanism by which the NLRP3 inflammasome initiated cancer cell death was not elucidated. The present study aimed to investigate the effect of NLRP3 inflammasome activation on cell death pathways and autophagy of HCC cells. First, we observed an increasing mortality in E2-treated HCC cells, and then apoptotic and pyroptotic cell death were both detected. The mortality of HCC cells was largely reversed by the caspase 1 antagonist, YVAD-cmk, suggesting that E2-induced cell death was associated with caspase 1-dependent pyroptosis. Second, the key role of the NLRP3 inflammasome in autophagy of HCC cells was assessed by E2-induced activation of the NLRP3 inflammasome, and we demonstrated that autophagy was inhibited by the NLRP3 inflammasome via the E2/ERβ/AMPK/mTOR pathway. Last, the interaction of pyroptosis and autophagy was confirmed by flow cytometry methods. We observed that E2-induced pyroptosis was dramatically increased by 3-methyladenine (3-MA) treatment, which was abolished by YVAD-cmk treatment, suggesting that caspase 1-dependent pyroptosis was negatively regulated by autophagy. In conclusion, E2-induced activation of the NLRP3 inflammasome may serve as a suppressor in HCC progression, as it triggers pyroptotic cell death and inhibits protective autophagy.
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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.