ArticleScientific reports2016
Pharmacoproteomic analysis reveals that metapristone (RU486 metabolite) intervenes E-cadherin and vimentin to realize cancer metastasis chemoprevention.
Article in Scientific reports, 2016. 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, 30 citations in OpenAlex.
- Reduced Proline-Rich Tyrosine Kinase 2 Promotes Tumor Metastasis by Activating Epithelial-Mesenchymal Transition in Colorectal Cancer.Digestive diseases and sciences · 2024Article
- Effect of Mifepristone on Migration and Proliferation of Oral Cancer Cells.International journal of molecular sciences · 2024Article
- Interactive mechanisms between caveolin-1 and actin filaments or vimentin intermediate filaments instruct cell mechanosensing and migration.Journal of molecular cell biology · 2023Article
- Cancer metastasis chemoprevention prevents circulating tumour cells from germination.Signal transduction and targeted therapy · 2022Review
- circPOLR1C Promotes the Development of Esophageal Cancer by Adsorbing miR-361-3p and Regulating Cancer Cell Apoptosis and Metastasis.Journal of oncology · 2022Article
- Monoamine Oxidase (MAO) as a Potential Target for Anticancer Drug Design and Development.Molecules (Basel, Switzerland) · 2021Review
- Mifepristone Treatment Promotes Testicular Leydig Cell Tumor Progression in Transgenic Mice.Cancers · 2020Article
- The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- The role of monoamine oxidase A in HPV-16 E7-induced epithelial-mesenchymal transition and HIF-1α protein accumulation in non-small cell lung cancer cells.International journal of biological sciences · 2020Article
- Molecular mechanisms underlying mifepristone's agonistic action on ovarian cancer progression.EBioMedicine · 2019Article
- Co-delivery of sorafenib and metapristone encapsulated by CXCR4-targeted PLGA-PEG nanoparticles overcomes hepatocellular carcinoma resistance to sorafenib.Journal of experimental & clinical cancer research : CR · 2019Article
- Proteomic Technology "Lens" for Epithelial-Mesenchymal Transition Process Identification in Oncology.Analytical cellular pathology (Amsterdam) · 2019Review
- RU486 Metabolite Inhibits CCN1/Cyr61 Secretion by MDA-MB-231-Endothelial Adhesion.Frontiers in pharmacology · 2019Article
- Suppression of the Smurf1 Expression Inhibits Tumor Progression in Gliomas.Cellular and molecular neurobiology · 2018Article
- Increased expression of monoamine oxidase A is associated with epithelial to mesenchymal transition and clinicopathological features in non-small cell lung cancer.Oncology letters · 2018Article
- Sex-related pharmacokinetic differences and mechanisms of metapristone (RU486 metabolite).Scientific reports · 2017Article
- Metapristone (RU486 metabolite) suppresses NSCLC by targeting EGFR-mediated PI3K/AKT pathway.Oncotarget · 2017Article
- EMT and inflammation: inseparable actors of cancer progression.Molecular oncology · 2017Review
- Secretome of tumor-associated leukocytes augment epithelial-mesenchymal transition in positive lymph node breast cancer patients via activation of EGFR/Tyr845 and NF-κB/p65 signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metapristone is the most predominant biological active metabolite of mifepristone, and being developed as a novel cancer metastasis chemopreventive agent by us. Despite its prominent metastasis chemopreventive effect, the underlying mechanism remains elusive. Our study, for the first time, demonstrated that metapristone had the ability to prevent breast cancer cells from migration, invasion, and interfere with their adhesion to endothelial cells. To explore the underlying mechanism of metapristone, we employed the iTRAQ technique to assess the effect of metapristone on MDA-MB-231 cells. In total, 5,145 proteins were identified, of which, 311 proteins showed significant differences in metapristone-treated cells compared to the control group (P-value < 0.05). Bioinformatic analysis showed many differentially expressed proteins (DEPs) functionally associated with post-translational modification, chaperones, translation, transcription, replication, signal transduction, etc. Importantly, many of the DEPs, such as E-cadherin, vimentin, TGF-β receptor I/II, smad2/3, β-catenin, caveolin, and dystroglycan were associated with TGF-β and Wnt signaling pathways, which were also linked to epithelial-to-mesenchymal transition (EMT) process. Further validation of the epithelial marker "E-caderin" and mesenchymal marker "vimetin" were carried out using immunoblot and immunofluorescence. These results have revealed a novel mechanism that metapristone-mediated metastasis chemoprevention is through intervening the EMT-related signaling pathways.
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