MoMaTEC1606
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Mari Halle
PROVIDER: E-MTAB-5017 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2013-01-24 | E-MTAB-1358 | biostudies-arrayexpress
Project description:Expression profiling of prostate EPT1 cells transducted with two types of miRNAs (miR-182, miR-203) and RNAi clones knocking down SNAI2.
2012-04-27 | E-MTAB-1107 | biostudies-arrayexpress
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.
2010-05-01 | E-TABM-949 | biostudies-arrayexpress
Project description:In an experimental model of tumor dormancy, heat shock protein 27 (HSP27) was up-regulated in angiogenic human breast cancer cells when compared with non-angiogenic cells. Stable down-regulation of HSP27 in angiogenic tumor cells was followed by long-term tumor dormancy in vivo and associated with reduced intra-tumoral endothelial cell proliferation, decreased secretion of VEGF and bFGF from tumor cells, and increased expression of thrombospondin-1. Phosphorylation of the transcription factor STAT3 and nuclear expression of NFκB were reduced following suppression of HSP27. In contrast, tumor cell proliferation and apoptosis were not affected. By clinical validation, high HSP27 expression was associated with markers of aggressive tumors and decreased survival in breast cancer and melanoma patients. Our present findings suggest a link between HSP27 and dormancy through tumor-vascular interactions. Targeting HSP27, a multifunctional cytoprotective protein, might offer a novel strategy in cancer treatment.
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2010-09-01 | E-MEXP-2788 | biostudies-arrayexpress
Project description:Tumor hypoxia is relevant for tumor growth, metabolism and epithelial-to-mesenchymal transition (EMT). We report that hyperbaric oxygen (HBO) treatment induced mesenchymal-to-epithelial transition (MET) in a dimetyl-α-benzantracene induced mammary rat adenocarcinoma model, and the MET was associated with extensive coordinated gene expression changes and less aggressive tumors. One group of tumor bearing rats was exposed to HBO (2 bar, pO2 = 2 bar, 4 exposures à 90 minutes), whereas the control group was housed under normal atmosphere (1 bar, pO2 = 0.2 bar). Treatment effects were determined by assessment of tumor growth, tumor vascularisation, tumor cell proliferation, cell death, collagen fibrils and gene expression profile. Tumor growth was significantly reduced (~16%) after HBO treatment compared to day 1 levels, whereas control tumors increased almost 100 % in volume. Significant decreases in tumor cell proliferation, tumor blood vessels and collagen fibrils, together with an increase in cell death, are consistent with tumor growth reduction and tumor stroma influence after hyperoxic treatment. Gene expression profiling showed that HBO induced MET with coordinated expression of gene modules involved in cell junctions and attachments together with a shift towards non-tumorigenic metabolism. This leads to more differentiated and less aggressive tumors, and indicates that oxygen per se might be an important factor in the â??switchesâ?? of EMT and MET in vivo. HBO treatment also attenuated tumor growth and changed tumor stroma, by targeting the vascular system, having anti-proliferative and pro-apoptotic effects.
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2011-04-15 | E-MEXP-3042 | biostudies-arrayexpress