ArticleMolecules (Basel, Switzerland)2019
Dioscin Inhibits the Invasion and Migration of Hepatocellular Carcinoma HepG2 Cells by Reversing TGF-β1-Induced Epithelial-Mesenchymal Transition.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Research status and challenges of anti-tumor effects of natural saponins and their combination therapy.Journal of the Egyptian National Cancer Institute · 2026Review
- Therapeutic potential of diosgenin in hepatocellular carcinoma through molecular mechanisms and nanodelivery strategies.Discover oncology · 2026Review
- Dioscin in liver diseases: pharmacological mechanisms, translational potential and future perspectives.Frontiers in pharmacology · 2026Review
- Dioscin alleviates the dysfunction of fibroblast-like synoviocytes by circ_0008267/miR-942-5p/FKBP5 axis during rheumatoid arthritis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Article
- Bioactive Metabolites ofFoods (Basel, Switzerland) · 2025Review
- Integrating experimental and network pharmacology to explore the pharmacological mechanisms of Dioscin against glioblastoma.Open medicine (Warsaw, Poland) · 2025Article
- Dioscin Impedes Proliferation, Metastasis and Enhances Autophagy of Gastric Cancer Cells via Regulating the USP8/TGM2 Pathway.Molecular biotechnology · 2024Article
- Targeting cell death mechanisms: the potential of autophagy and ferroptosis in hepatocellular carcinoma therapy.Frontiers in immunology · 2024Review
- Targeting and regulation of autophagy in hepatocellular carcinoma: revisiting the molecular interactions and mechanisms for new therapy approaches.Cell communication and signaling : CCS · 2023Review
- Shen Qi Wan-Containing Serum Alleviates Renal Interstitial Fibrosis via Restraining Notch1-Mediated Epithelial-Mesenchymal Transition.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Epithelial-to-Mesenchymal Transition in Metastasis: Focus on Laryngeal Carcinoma.Biomedicines · 2022Review
- Targeting transforming growth factor-β signalling for cancer prevention and intervention: Recent advances in developing small molecules of natural origin.Clinical and translational medicine · 2022Review
- Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- Ailanthoidol, a Neolignan, Suppresses TGF-β1-Induced HepG2 Hepatoblastoma Cell Progression.Biomedicines · 2021Article
- Exploring the Biological Mechanism of Huang Yam in Treating Tumors and Preventing Antitumor Drug-Induced Cardiotoxicity Using Network Pharmacology and Molecular Docking Technology.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Chemerin Isoform-Specific Effects on Hepatocyte Migration and Immune Cell Inflammation.International journal of molecular sciences · 2020Article
- Selective Targeting of αvβ5 Integrin in HepG2 Cell Line by RGDechi15D Peptide.Molecules (Basel, Switzerland) · 2020Article
- Review
- Network Pharmacology and Experimental Evidence Reveal Dioscin Suppresses Proliferation, Invasion, and EMT via AKT/GSK3b/mTOR Signaling in Lung Adenocarcinoma.Drug design, development and therapy · 2020Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Dioscin is a natural steroidal saponin that can be isolated from Chinese medicine, such as Dioscoreae rhizoma. It has wild range of pharmacological activities such as hepatoprotection, a lipid-lowering effect, and anti-inflammation. Recently, mounting studies reported the anticancer effect of dioscin on a variety of tumor cells. However, the potential effect of dioscin on the epithelial-mesenchymal transition (EMT) of HepG2 cells is unclear. In the present study, dioscin was identified to inhibit transforming growth factor-β1 (TGF-β1) and induced invasive and migratory behavior of HepG2 cells. Consistently, the expression of the epithelial marker E-cadherin and gap junction proteins increased following dioscin treatment, while mesenchymal markers decreased, including N-cadherin, Vimentin, Snail, and Slug. Furthermore, we discovered that TGF-β1 induces phosphorylation of JNK, p38, and Erk, whereas the activation of these kinases was reversed by dioscin treatment in a dose-dependent manner. With the addition of Asiatic acid, a p38 activator, the inhibitory effect of dioscin on EMT was reversed. Taken together, these data indicated that dioscin inhibits EMT in HepG2 cells, which is mediated in large part by inhibition of the p38-MAPK signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.