ArticleCell death & disease2024
Arsenic trioxide augments immunogenic cell death and induces cGAS-STING-IFN pathway activation in hepatocellular carcinoma.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- ATO alleviates T-cell immunosuppression by inducing apoptosis-associated secretion of IL-2 in FLT3-ITD-mutated acute myeloid leukemia.Translational oncology · 2026Article
- Navitoclax-encapsulated dual pH-responsive copolymeric nanoparticles improves hepatocellular carcinoma treatment with induction of apoptosis and immune activation.Journal of nanobiotechnology · 2026Article
- Integrated Elementomics-Genomics-Metabolomics Analysis Reveals Plasma Biomarker Networks and Diagnostic Potential for Gastric Cancer.Metabolites · 2026Article
- Renaissance of Traditional Mineral Drugs in Cancer: Advanced Delivery Strategies and Bioengineering Approaches.Pharmaceutics · 2026Review
- Localised Autophagy Inhibition by Nanodiamonds Potentiates Arsenic Therapy With Favourable Safety Profile in Solid Tumours.Cell proliferation · 2026Article
- Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026Review
- Prognostic significance and immune correlation of STING expression and promoter methylation in renal cell carcinoma.Scientific reports · 2026Article
- Astragalus Polysaccharides Induce Immunogenic Cell Death in Melanoma: A Mechanism Mediated by cGAS/STING Activation via Intratumoral Microbiota Modulation.Cancer medicine · 2026Article
- Biomimetic Nanomedicine for Senescence-Modulated Immune Activation Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cucurbitacin B Inhibits Hepatocellular Carcinoma by Inducing Ferroptosis and Activating the cGAS-STING Pathway.Current issues in molecular biology · 2026Article
- Post-Translational Modification Networks in Ferroptosis: Orchestrating Defense, Drug Resistance, and Therapeutic Opportunities in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2026Review
- Spatiotemporal control of immunogenic cell death: rewiring tumor-immune dialogues for next-generation immunotherapy.Frontiers in immunology · 2026Review
- Pirenzepine exhibits anti-prostate cancer activity and enhances checkpoint inhibitor-based immunotherapy by targeting STING.European journal of medical research · 2025Article
- Arsenic Trioxide Underpins Delayed Neuroinflammation and Impaired Synaptic Integrity involving Integrative Stress Response Signaling.bioRxiv : the preprint server for biology · 2025Article
- Arsenic trioxide-based nanoparticles for enhanced chemotherapy by activating pyroptosis.Acta pharmaceutica Sinica. B · 2025Article
- Therapeutic targeting of cell death-immune crosstalk in cancer to rewire the tumor immune microenvironment.Molecular cancer · 2025Review
- The role of cGAS-STING signaling pathway in ferroptosis.Journal of advanced research · 2025Review
- Tetraarsenic Hexoxide Enhanced the Anticancer Effects ofInternational journal of molecular sciences · 2025Article
- The cGAS-STING pathway: a dual regulator of immune response in cancer and therapeutic implications.Journal of translational medicine · 2025Review
- The spatiotemporal heterogeneity of reactive oxygen species in the malignant transformation of viral hepatitis to hepatocellular carcinoma: a new insight.Cellular & molecular biology letters · 2025Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The treatment of hepatocellular carcinoma (HCC) is particularly challenging due to the inherent tumoral heterogeneity and easy resistance towards chemotherapy and immunotherapy. Arsenic trioxide (ATO) has emerged as a cytotoxic agent effective for treating solid tumors, including advanced HCC. However, its effectiveness in HCC treatment remains limited, and the underlying mechanisms are still uncertain. Therefore, this study aimed to characterize the effects and mechanisms of ATO in HCC. By evaluating the susceptibilities of human and murine HCC cell lines to ATO treatment, we discovered that HCC cells exhibited a range of sensitivity to ATO treatment, highlighting their inherent heterogeneity. A gene signature comprising 265 genes was identified to distinguish ATO-sensitive from ATO-insensitive cells. According to this signature, HCC patients have also been classified and exhibited differential features of ATO response. Our results showed that ATO treatment induced reactive oxygen species (ROS) accumulation and the activation of multiple cell death modalities, including necroptosis and ferroptosis, in ATO-sensitive HCC cells. Meanwhile, elevated tumoral immunogenicity was also observed in ATO-sensitive HCC cells. Similar effects were not observed in ATO-insensitive cells. We reported that ATO treatment induced mitochondrial injury and mtDNA release into the cytoplasm in ATO-sensitive HCC tumors. This subsequently activated the cGAS-STING-IFN axis, facilitating CD8
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