ArticleRedox report : communications in free radical research2024
Jaceosidin induces apoptosis and inhibits migration in AGS gastric cancer cells by regulating ROS-mediated signaling pathways.
Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Multi-Target Antitumor Effects of Natural Products and Approved Drug Repurposing in Non-Small Cell Lung Cancer: Advances in Mechanisms, Combination Regimens, Delivery System Optimization, and Clinical Challenges.International journal of molecular sciences · 2026Review
- Redox-regulated cell death in gastric cancer: Molecular insights and therapeutic opportunities.Journal of physiology and biochemistry · 2026Review
- Preliminary exploration of the putative function of SF3A2 in clear cell renal cell carcinoma.Molecular medicine reports · 2026Article
- Jaceidin Suppresses Melanoma Metastasis by Modulating ERK, JNK Pathways and Extracellular Matrix Degradation Proteins.Journal of cellular and molecular medicine · 2026Article
- Connexin Restrains EMT by Dual-Domain Mechanisms to Preserve Epithelial Identity.Research square · 2025Article
- [Elevated TMCO1 expression in gastric cancer is associated poor prognosis and promotes malignant phenotypes of tumor cells by inhibiting apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- HIF-1α Promotes the Confined Migration of Gastric Cancer Cells by Modulating Phosphatidylcholine Metabolism.Journal of cellular and molecular medicine · 2025Article
- Mechanistic Study of Jaceosidin in Regulating Secondary Inflammation After Spinal Cord Injury in Mouse by Inhibiting PKM2 Activity.Neuromolecular medicine · 2025Article
- Immunometabolism and oxidative stress: roles and therapeutic strategies in cancer and aging.npj aging · 2025Review
- Identification and validation of T cell senescence-related prognostic genes in gastric carcinoma and investigation of their potential regulatory mechanisms.Discover oncology · 2025Article
- Natural Compounds in Cancer Therapy: Revealing the Role of Flavonoids in Renal Cell Carcinoma Treatment.Biomolecules · 2025Review
- AsCurrent issues in molecular biology · 2025Article
- Therapeutic potential of flavonoids in gastrointestinal cancer: Focus on signaling pathways and improvement strategies (Review).Molecular medicine reports · 2025Review
- Mechanistic Insights into Flavonoid Subclasses as Cardioprotective Agents Against Doxorubicin-Induced Cardiotoxicity: A Comprehensive Review.Drug design, development and therapy · 2025Review
- Article
- Inhibition of mitochondrial OMA1 ameliorates osteosarcoma tumorigenesis.Cell death & disease · 2024Article
- [Kuwanon G inhibits growth, migration and invasion of gastric cancer cells by regulating the PI3K/AKT/mTOR pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Elucidation of Anti-Obesity Mechanisms of Phenolics inLife (Basel, Switzerland) · 2024Article
- Article
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8 authors.
Funding
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Abstract
Jaceosidin (JAC) is a natural flavonoid with anti-oxidant and other pharmacological activities; however, its anti-cancer mechanism remains unclear. We investigated the mechanism of action of JAC in gastric cancer cells. Cytotoxicity and apoptosis assays showed that JAC effectively killed multiple gastric cancer cells and induced apoptosis in human gastric adenocarcinoma AGS cells via the mitochondrial pathway. Network pharmacological analysis suggested that its activity was linked to reactive oxygen species (ROS), AKT, and MAPK signaling pathways. Furthermore, JAC accumulated ROS to up-regulate p-JNK, p-p38, and IκB-α protein expressions and down-regulate the p-ERK, p-STAT3, and NF-κB protein expressions. Cell cycle assay results showed that JAC accumulated ROS to up-regulate p21 and p27 protein expressions and down-regulate p-AKT, CDK2, CDK4, CDK6, Cyclin D1, and Cyclin E protein expressions to induce G0/G1 phase arrest. Cell migration assay results showed JAC accumulated ROS to down-regulate Wnt-3a, p-GSK-3β, N-cadherin, and β-catenin protein expressions and up-regulate E-cadherin protein expression to inhibit migration. Furthermore, N-acetyl cysteine pre-treatment prevented the change of these protein expressions. In summary, JAC induced apoptosis and G0/G1 phase arrest and inhibited migration through ROS-mediated signaling pathways in AGS cells.
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