ArticleScientific reports2018
Nemopilema nomurai jellyfish venom exerts an anti-metastatic effect by inhibiting Smad- and NF-κB-mediated epithelial-mesenchymal transition in HepG2 cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Venom-Derived Enzyme Inhibitors as Anticancer Agents: Structure-Activity Relationships, Molecular Targets and Mechanistic Insights.Molecules (Basel, Switzerland) · 2026Review
- Identification of New Angiotensin-Converting Enzyme Inhibitory Peptides Isolated from the Hydrolysate of the Venom ofToxins · 2024Article
- Exploring the Efficacy of Hydroxybenzoic Acid Derivatives in Mitigating Jellyfish Toxin-Induced Skin Damage: Insights into Protective and Reparative Mechanisms.Marine drugs · 2024Article
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- Developing natural marine products for treating liver diseases.World journal of clinical cases · 2022Review
- Ailanthoidol, a Neolignan, Suppresses TGF-β1-Induced HepG2 Hepatoblastoma Cell Progression.Biomedicines · 2021Article
- Nomad JellyfishMolecules (Basel, Switzerland) · 2021Article
- Protective effect of epigallocatechin-3-gallate (EGCG) on toxic metalloproteinases-mediated skin damage induced by Scyphozoan jellyfish envenomation.Scientific reports · 2020Article
- A Brief Review about the Role of Nanomaterials, Mineral-Organic Nanoparticles, and Extra-Bone Calcification in Promoting Carcinogenesis and Tumor Progression.Biomedicines · 2019Review
- Calcium Carbonate Nanoparticles Can Activate the Epithelial⁻Mesenchymal Transition in an Experimental Gastric Cancer Model.Biomedicines · 2019Article
- Targeting E-cadherin expression with small molecules for digestive cancer treatment.American journal of translational research · 2019Review
- Article
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Authors and funding
13 authors at 4 institutions in 1 country.
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Abstract
Epithelial-mesenchymal transition (EMT) is a key initial step in metastasis for malignant cancer cells to obtain invasive and motile properties. Inhibiting EMT has become a new strategy for cancer therapy. In our previous in vivo study, Nemopilema nomurai jellyfish venom (NnV) -treated HepG2 xenograft mice group showed that E-cadherin expression was strongly detected compared with non-treated groups. Therefore, this study aimed to determine whether NnV could inhibit the invasive and migratory abilities of HepG2 human hepatocellular carcinoma cells and to examine its effect on EMT. Our results revealed that transforming growth factor (TGF)-β1 induced cell morphological changes and downregulated E-cadherin and β-catenin expression, but upregulated N-cadherin and vimentin expression through the Smad and NF-κB pathways in HepG2 cells. Treatment of TGF-β1-stimulated HepG2 cells with NnV reversed the EMT-related marker expression, thereby inhibiting cell migration and invasion. NnV also significantly suppressed the activation of p-Smad3, Smad4, and p-NF-κB in a dose-dependent manner. These data indicated that NnV can significantly suppress cell migration and invasion by inhibiting EMT in HepG2 cells, and therefore might be a promising target for hepatocellular carcinoma therapeutics.
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