MoMaTEC1606
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Mari Halle
PROVIDER: E-MTAB-5017 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Background: The loss of epithelial characteristics and the acquisition of a migratory phenotype, referred to as epithelial to mesenchymal transition (EMT), is a crucial event in tumor metastasis. A better defined cell culture model for the study of EMT and its role in prostate carcinogenesis has been a challenge. Our previous work reported an EMT model based on primary prostate epithelial cells (EP156T) which gave rise to cells with mesenchymal phenotype (EPT1) without malignant transformation. Here, we present an extension of this model to stepwise malignant transformation in relation to EMT and gene expression reprogramming. Results: To achieve transformed prostate cells, EPT1 cells were kept growing in extended saturation density culture to select for cells overriding quiescence. Foci formed in EPT1 cells in 4 weeks. Cells from the foci can form robust colonies in soft agar suggesting malignant transformation. The transformed cells were named EPT2. In this stepwise transformation model, EPT2 cells showed much higher abilities to proliferation at confluence, higher resistance to apoptosis, and much lower dependence on serum and exogenous growth factors than EP156T and EPT1 cells. When EP156T and EPT1 cells at different passages were compared, only EPT1 cells at later passage but not EP156T cells could be induced to malignant transformation by high density culture. Microarray expression profiling showed that EMT and transformation were strongly connected at the gene expression level, suggesting that EMT makes EPT1 cells at later passage more susceptible to transformation induction. Conclusions: Our findings provide a novel stepwise transformation model in which EMT can emerge not only independent of transformation, but also can promote subsequent malignant transformation in prostate carcinogenesis. Dynamic changes of a core set of genes are involved in both EMT and subsequent malignant transformation.
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