ArticleJournal of translational medicine2023
Mitochondrial ROS driven by NOX4 upregulation promotes hepatocellular carcinoma cell survival after incomplete radiofrequency ablation by inducing of mitophagy via Nrf2/PINK1.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 54 citations in OpenAlex.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- NRF2-CDH6-CEBPD axis suppresses ferroptosis and drives cisplatin resistance in non-small cell lung cancer.Journal of cell communication and signaling · 2026Article
- Metabolism, autophagy, and cell death: The triangular axis in tumor survival and therapeutic resistance.Redox biology · 2026Review
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- FABP5 confers resistance to drug-induced ROS toxicity in cervical cancer cell lines by suppressing the PPARγ/CPT1A signaling pathway.Discover oncology · 2026Article
- Regulation of autophagy by the p53 family and the implications for cancer therapies.Discover oncology · 2026Review
- Advances in mitophagy research in hepatocellular carcinoma: mechanisms and therapeutic implications.Journal of gastrointestinal oncology · 2026Review
- Radiofrequency Fields at 2.45 GHz Reprogram Mitochondria-Lysosome Crosstalk and Modulate the Survival/Death of Macrophages Exposed to LPS and/or the SARS-CoV-2 Spike Protein.International journal of molecular sciences · 2026Article
- Targeting PTDSS1 to modulate GSH synthesis triggers mitophagy and induces ferroptosis in esophageal squamous cell carcinoma cells.Cell death & disease · 2026Article
- Ipriflavone FromMedComm · 2026Article
- Article
- Lycopene mitigates T-2 toxin-induced hepatic ferroptosis by targeting the Nrf2/mitophagy axis in mice.NPJ science of food · 2026Article
- NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.Frontiers in immunology · 2026Article
- Renoprotective actions of puerarin and the prospects of kidney-targeted nanodelivery.Frontiers in pharmacology · 2026Review
- Enhanced glucose uptake promotes the survival of hepatocellular carcinoma cells following incomplete radiofrequency ablation.Molecular & cellular oncology · 2026Article
- The Evolving Landscape of Hepatocellular Carcinoma Therapy: From Conventional Modalities to TME-Responsive Prodrug Design Strategies.Drug design, development and therapy · 2026Review
- The Role of Mitochondrial Dysfunction in Hepatocellular Carcinoma: From Pathogenesis and Drug Resistance to Targeted Therapeutic Strategies.Journal of hepatocellular carcinoma · 2026Review
- Tanshinone IIA inhibits heat-induced growth of p53-mutant Huh-7 hepatocellular carcinoma by modulating osmotic homeostasis and glycolysis through targeting ALDH7A1.Cell death discovery · 2025Article
- Astragaloside IV Ameliorates Cerebral Ischemic-Reperfusion Injury via Improving Mitochondrial Function and Inhibiting Neuronal Apoptosis.Current issues in molecular biology · 2025Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe recurrence of hepatocellular carcinoma (HCC) after radiofrequency ablation (RFA) remains a major clinical problem. Cells that survive the sublethal heat stress that is induced by incomplete RFA are the main source of HCC relapse. Heat stress has long been reported to increase intracellular reactive oxygen species (ROS) generation. Although ROS can induce apoptosis, a pro-survival effect of ROS has also been demonstrated. However, the role of ROS in HCC cells exposed to sublethal heat stress remains unclear.
methodsHepG2 and HuH7 cells were used for this experiment. Insufficient RFA was performed in cells and in a xenograft model. ROS and antioxidant levels were measured. Apoptosis was analyed by Annexin-V/PI staining and flow cytometry. Protein expression was measured using western blotting. Colocalization of lysosomes and mitochondria was analyzed to assess mitophagy. Corresponding activators or inhibitors were applied to verify the function of specific objectives.
resultsHere,we showed that sublethal heat stress induced a ROS burst, which caused acute oxidative stress. This ROS burst was generated by mitochondria, and it was initiated by upregulated NOX4 expression in the mitochondria. N-acetylcysteine (NAC) decreased HCC cell survival under sublethal heat stress conditions in vivo and in vitro. NOX4 triggers the production of mitochondrial ROS (mtROS), and NOX4 inhibitors or siNOX4 also decreased HCC cell survival under sublethal heat stress conditions in vitro. Increased mtROS trigger PINK1-dependent mitophagy to eliminate the mitochondria that are damaged by sublethal heat stress and to protect cells from apoptosis. Nrf2 expression was elevated in response to this ROS burst and mediated the ROS burst-induced increase in PINK1 expression after sublethal heat stress.
conclusionThese data confirmed that the ROS burst that occurs after iRFA exerted a pro-survival effect. NOX4 increased the generation of ROS by mitochondria. This short-term ROS burst induced PINK1-dependent mitophagy to eliminate damaged mitochondria by increasing Nrf2 expression.
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