ArticleBioMed research international2016
Emodin Inhibits the Epithelial to Mesenchymal Transition of Epithelial Ovarian Cancer Cells via ILK/GSK-3
Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action.International journal of molecular sciences · 2024Review
- A nanoscale natural drug delivery system for targeted drug delivery against ovarian cancer: action mechanism, application enlightenment and future potential.Frontiers in immunology · 2024Review
- Anti-Cancer Potential of Phytochemicals: The Regulation of the Epithelial-Mesenchymal Transition.Molecules (Basel, Switzerland) · 2023Review
- The Role of Natural and Semi-Synthetic Compounds in Ovarian Cancer: Updates on Mechanisms of Action, Current Trends and Perspectives.Molecules (Basel, Switzerland) · 2023Review
- Synergistic effect of Tripterygium glycosides and cisplatin on drug-resistant human epithelial ovarian cancer via ILK/GSK3β/Slug signal pathway.American journal of translational research · 2022Article
- The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers.International journal of biological sciences · 2022Review
- Advances in the study of emodin: an update on pharmacological properties and mechanistic basis.Chinese medicine · 2021Review
- Mechanisms and Advances in Anti-Ovarian Cancer with Natural Plants Component.Molecules (Basel, Switzerland) · 2021Review
- Regulation of angiogenesis by microRNAs in cancer.Molecular medicine reports · 2021Review
- Review
- The role of glycogen synthase kinase 3 (GSK3) in cancer with emphasis on ovarian cancer development and progression: A comprehensive review.Bosnian journal of basic medical sciences · 2021Review
- Emodin Reverses the Epithelial-Mesenchymal Transition of Human Endometrial Stromal Cells by Inhibiting ILK/GSK-3β Pathway.Drug design, development and therapy · 2020Article
- Overexpression of microRNA-195-5p reduces cisplatin resistance and angiogenesis in ovarian cancer by inhibiting the PSAT1-dependent GSK3β/β-catenin signaling pathway.Journal of translational medicine · 2019Article
- Emodin Inhibits Colon Cancer Cell Invasion and Migration by Suppressing Epithelial-Mesenchymal Transition via the Wnt/β-Catenin Pathway.Oncology research · 2019Article
- MicroR-542-3p can mediateAging · 2019Article
- Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer.Cancer biomarkers : section A of Disease markers · 2018Article
- EMT: Present and future in clinical oncology.Molecular oncology · 2017Review
- Expression of Clonorchis sinensis GIIIsPLAParasitology research · 2017Article
- Therapy Effects of Wogonin on Ovarian Cancer Cells.BioMed research international · 2017Article
- Emodin suppresses proliferation, migration and invasion in ovarian cancer cells by down regulating ILK in vitro and in vivo.OncoTargets and therapy · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. Despite the anticancer capabilities of emodin observed in many cancers, including EOC, the underlying molecular mechanism remains to be elucidated. A crucial link has been discovered between the acquisition of metastatic traits and the epithelial-mesenchymal transition (EMT). The present study aimed to determine whether emodin could inhibit the EMT of EOC cells and explore the underlying mechanism. The CCK-8 assay and transwell assay showed that emodin effectively repressed the abilities of proliferation, invasion, and migration in A2780 and SK-OV-3 cells. The Western blot showed that emodin upregulated epithelial markers (E-cadherin and Claudin) while it downregulated mesenchymal markers (N-cadherin and Vimentin) and transcription factor (Slug) in a dose-dependent fashion. After transfection of siRNA-Slug, both Slug and N-cadherin were downregulated in EOC cells while E-cadherin was upregulated, which was intensified by emodin. Besides, emodin decreased the expression of ILK, p-GSK-3
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