Emodin Inhibits the Epithelial to Mesenchymal Transition of Epithelial Ovarian Cancer Cells via ILK/GSK-3β/Slug Signaling Pathway.
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 trai...
| Publicado en: | BioMed Research International Vol. 2016; pp. 1 - 17 |
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| Autores principales: | , , , , , |
| Formato: | pictorial research tables/charts Journal Article |
| Publicado: |
Wiley-Blackwell
12/20/2016
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=120314714&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 120314714 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 23146133 FT2T jtl: BioMed Research International issn: 23146133 maglogo: N pubinfo: dt: 12/20/2016 vid: 2016 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 120314714 120314714 120314714 10.1155/2016/6253280 120314714 ppf: 1 ppct: 16 formats: fmt: @attributes: type: P tig: atl: Emodin Inhibits the Epithelial to Mesenchymal Transition of Epithelial Ovarian Cancer Cells via ILK/GSK-3β/Slug Signaling Pathway. aug: au: Lu, Jingjing Xu, Ying Wei, Xuan Zhao, Zhe Xue, Jing Liu, Peishu affil: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan, Shandong 250012, China sug: subj: Cascara Administration and Dosage Fetal Development Drug Effects Ovarian Neoplasms Drug Therapy Neoplasms, Glandular and Epithelial Drug Therapy Signal Transduction Drug Effects Protein Kinases Drug Effects Transcription Factors Drug Effects Cell Line, Tumor Human Cell Culture Techniques Neoplasm Metastasis Biological Assay Blotting, Western Cell Adhesion Molecules Cytoskeletal Proteins Genetic Techniques RNA Protein Kinase Inhibitors Administration and Dosage Cell Migration Assays Cell Physiology Drug Effects Descriptive Statistics P-Value Data Analysis Software One-Way Analysis of Variance T-Tests Funding Source ab: 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-3β, β-catenin, and Slug. Transfection of siRNA-ILK also achieved the same effects, which was further strengthened by following emodin treatment. Nevertheless, SB216763, an inhibitor of GSK-3β, could reverse the effects of emodin except for ILK expression. These findings suggest that emodin inhibited the EMT of EOC cells via ILK/GSK-3β/Slug signaling pathway. pubtype: Academic Journal doctype: pictorial research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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