ArticleClinical and translational medicine2021
Arsenic trioxide induces differentiation of cancer stem cells in hepatocellular carcinoma through inhibition of LIF/JAK1/STAT3 and NF-kB signaling pathways synergistically.
Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 63 citations in OpenAlex.
- Synergistic regulation of TGF-β1/Smad2/3 signaling and inflammatory pathways via SA/NAC-based nanoplatforms: a novel strategy to enhance anti-fibrotic therapeutic outcomes in idiopathic pulmonary fibrosis.Journal of nanobiotechnology · 2026Article
- The epigenetic regulator SETDB1 as a key component of cancer stem cells and drug resistance in primary liver cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Investigating the Mechanisms of Combined Therapy for MCF-7 Breast Cancer Cells Using Arsenic Trioxide and Resveratrol through Network Pharmacology.Phenomics (Cham, Switzerland) · 2025Article
- Targeting ICAM1 through LIF-mediated NF-κB/JAK2-STAT3 crosstalk protects nucleus pulposus from IL-1β-driven pyroptosis to ameliorate intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2025Article
- Synergic chemotherapeutic effects of docetaxel and carboplatin show cytotoxic and apoptotic effects in liver cancer nursing care: Role of oxidative stress and hemocompatibility.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The concurrent silencing of Tim-3 and STAT-3 promotes tumor regression both in vitro and in ovo.BMC cancer · 2025Article
- Hepatocellular carcinoma stem cells: the current state of small molecule-based inhibitors.Cell death & disease · 2025Review
- Patient-derived xenograft model: Applications and challenges in liver cancer.Chinese medical journal · 2025Review
- Article
- Targeted Therapy of Tumors and Cancer Stem Cells based on Oxidant-regulated Redox Pathway and its Mechanism.Current computer-aided drug design · 2025Review
- A bibliometric and visual analysis of Jak1 to explore trends and frontiers.Frontiers in oncology · 2025Review
- Study on the Mechanism of QRICH1 Mediating PRMT1 to Regulate the Arginine Methylation Modification of cGAS to Promote Arsenics-Induced Pyroptosis in Hepatocellular Carcinoma Cells.Journal of hepatocellular carcinoma · 2025Article
- Extinguishing the flames of inflammation: retardant effect of chlorquinaldol on NLRP3-driven diseases.Molecular medicine (Cambridge, Mass.) · 2024Article
- S100A8 promotes tumor progression by inducing phenotypic polarization of microglia through the TLR4/IL-10 signaling pathway in glioma.Journal of the National Cancer Center · 2024Article
- Insight into the mechanisms regulating liver cancer stem cells by hepatitis B virus X protein.Infectious agents and cancer · 2024Review
- Targeting catalase in cancer.Redox biology · 2024Review
- Multiple roles of arsenic compounds in phase separation and membraneless organelles formation determine their therapeutic efficacy in tumors.Journal of pharmaceutical analysis · 2024Review
- Versatile function of NF-ĸB in inflammation and cancer.Experimental hematology & oncology · 2024Review
- Arsenic trioxide augments immunogenic cell death and induces cGAS-STING-IFN pathway activation in hepatocellular carcinoma.Cell death & disease · 2024Article
- [High LINC00626 expression promotes esophagogastric junction adenocarcinoma metastasis: the mediating role of the JAK1/STAT3/KHSRP axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDifferentiation-inducing therapy for tumors is a strategy that aims to induce the differentiation and maturation of cancer stem cells (CSCs). The differentiation-inducing capacity of arsenic trioxide (ATO) in hepatocellular carcinoma (HCC) and the underlying mechanism were previously unknown.
methodsIn the present study, we explored the ATO-induced differentiation of CSCs in HCC by detecting the expression of CSC-related markers and tumorigenicity variation in vivo and in vitro. We developed a combined chemotherapeutic approach to HCC by characterizing the effects of combinatorial treatment with 5-fluorouracil (5-FU)/cisplatin and ATO in vitro and in patient-derived xenograft models. Changes in gene expression patterns were investigated by gene microarray analysis.
resultsATO effectively induced differentiation of CSCs by downregulation of CSC-related genes and suppression of tumorigenicity capability. Combinatorial treatment with ATO and 5-FU/cisplatin significantly enhanced therapeutic effects in HCC cells compared with the treatment with 5-FU/cisplatin alone. Synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways by ATO and 5-FU/cisplatin is a potential molecular mechanism underlying the differentiation effect.
conclusionsATO induced the differentiation of HCC CSCs and potentiated the cytotoxic effects of 5-FU/cisplatin through synergistic inhibition of the LIF/JAK1/STAT3 and NF-kB signaling pathways. These results offer new insights for the clinical treatment of HCC.
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