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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,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NT13573
MZ0
CEP Register
Digital library NLK
Full text - Article
Source
NLK
Free Medical Journals
from 2010
Freely Accessible Journals
from 2010
PubMed Central
from 2010
Europe PubMed Central
from 2010
Open Access Digital Library
from 2010-01-01
- MeSH
- Epithelial-Mesenchymal Transition physiology MeSH
- Phenotype MeSH
- Heterografts MeSH
- Nuclear Proteins biosynthesis MeSH
- Humans MeSH
- Mice, Nude MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- Prostatic Neoplasms genetics metabolism pathology MeSH
- Breast Neoplasms genetics metabolism pathology MeSH
- Proto-Oncogene Proteins c-mdm2 biosynthesis MeSH
- Proto-Oncogene Proteins biosynthesis MeSH
- Transfection MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't 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.
References provided by Crossref.org
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- $a 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.
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