2015
Slabáková, Eva; Kharaishvili, Gvantsa; Smějová, Monika; Pernicová, Zuzana; Suchánková, Tereza; Remšík, Ján; Lerch, Stanislav; Straková, Nicol; Bouchal, Jan; Král, Milan; Culig, Zoran; Kozubík, Alois; Souček, Karel
Opposite regulation of MDM2 and MDMX expression in acquisition of mesenchymal phenotype in benign and cancer cells. Journal Article
In: Oncotarget, vol. 6, no. 34, pp. 36156–36171, 2015, ISSN: 1949-2553, (Place: United States).
Abstract | Links | BibTeX | Tags: Animals, Breast Neoplasms/genetics/*metabolism/pathology, Cell Cycle Proteins, Cell Line, Epithelial-Mesenchymal Transition, Epithelial-Mesenchymal Transition/*physiology, Female, Heterografts, Humans, Male, MDM2/MDMX, Mice, Nuclear Proteins/*biosynthesis, Nude, Phenotype, prostate/breast cancer, Prostatic Neoplasms/genetics/*metabolism/pathology, Proto-Oncogene Proteins c-mdm2/*biosynthesis, Proto-Oncogene Proteins/*biosynthesis, Snai2/Slug, Transfection, Tumor, TWIST
@article{slabakova_opposite_2015,
title = {Opposite regulation of MDM2 and MDMX expression in acquisition of mesenchymal phenotype in benign and cancer cells.},
author = {Eva Slabáková and Gvantsa Kharaishvili and Monika Smějová and Zuzana Pernicová and Tereza Suchánková and Ján Remšík and Stanislav Lerch and Nicol Straková and Jan Bouchal and Milan Král and Zoran Culig and Alois Kozubík and Karel Souček},
doi = {10.18632/oncotarget.5392},
issn = {1949-2553},
year = {2015},
date = {2015-11-01},
journal = {Oncotarget},
volume = {6},
number = {34},
pages = {36156–36171},
abstract = {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.},
note = {Place: United States},
keywords = {Animals, Breast Neoplasms/genetics/*metabolism/pathology, Cell Cycle Proteins, Cell Line, Epithelial-Mesenchymal Transition, Epithelial-Mesenchymal Transition/*physiology, Female, Heterografts, Humans, Male, MDM2/MDMX, Mice, Nuclear Proteins/*biosynthesis, Nude, Phenotype, prostate/breast cancer, Prostatic Neoplasms/genetics/*metabolism/pathology, Proto-Oncogene Proteins c-mdm2/*biosynthesis, Proto-Oncogene Proteins/*biosynthesis, Snai2/Slug, Transfection, Tumor, TWIST},
pubstate = {published},
tppubtype = {article}
}