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Opposite regulation of MDM2 and MDMX expression in acquisition of mesenchymal phenotype in benign and cancer cells
E. Slabáková, G. Kharaishvili, M. Smějová, Z. Pernicová, T. Suchánková, J. Remšík, S. Lerch, N. Straková, J. Bouchal, M. Král, Z. Culig, A. Kozubík, K. Souček,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT13573
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Free Medical Journals
od 2010
Freely Accessible Journals
od 2010
PubMed Central
od 2010
Europe PubMed Central
od 2010
Open Access Digital Library
od 2010-01-01
PubMed
26416355
DOI
10.18632/oncotarget.5392
Knihovny.cz E-zdroje
- MeSH
- epitelo-mezenchymální tranzice fyziologie MeSH
- fenotyp MeSH
- heterografty MeSH
- jaderné proteiny biosyntéza MeSH
- lidé MeSH
- myši nahé MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- nádory prostaty genetika metabolismus patologie MeSH
- nádory prsu genetika metabolismus patologie MeSH
- protoonkogenní proteiny c-mdm2 biosyntéza MeSH
- protoonkogenní proteiny biosyntéza MeSH
- transfekce MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Plasticity of cancer cells, manifested by transitions between epithelial and mesenchymal phenotypes, represents a challenging issue in the treatment of neoplasias. Both epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) are implicated in the processes of metastasis formation and acquisition of stem cell-like properties. Mouse double minute (MDM) 2 and MDMX are important players in cancer progression, as they act as regulators of p53, but their function in EMT and metastasis may be contradictory. Here, we show that the EMT phenotype in multiple cellular models and in clinical prostate and breast cancer samples is associated with a decrease in MDM2 and increase in MDMX expression. Modulation of EMT-accompanying changes in MDM2 expression in benign and transformed prostate epithelial cells influences their migration capacity and sensitivity to docetaxel. Analysis of putative mechanisms of MDM2 expression control demonstrates that in the context of defective p53 function, MDM2 expression is regulated by EMT-inducing transcription factors Slug and Twist. These results provide an alternative context-specific role of MDM2 in EMT, cell migration, metastasis, and therapy resistance.
Citace poskytuje Crossref.org
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