Abstract
Epithelial to mesenchymal transition (EMT) is pivotal in tumor metastasis. 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. To promote prostate cell transformation, cells were maintained in saturation density cultures to select for cells overriding quiescence. Foci formed repeatedly following around 8 weeks in confluent EPT1 monolayers. Only later passage EPT1, but not EP156T cells of any passage, could form foci. Cells isolated from the foci were named EPT2 and formed robust colonies in soft agar, a malignant feature present neither in EP156T nor in EPT1 cells. EPT2 cells showed additional malignant traits in vitro, including higher ability to proliferate following confluence, higher resistance to apoptosis and lower dependence on exogenous growth factors than EP156T and EPT1 cells. Microarray profiling identified gene sets, many of which belong to cell junction modules, that changed expression from EP156T to EPT1 cells and continued to change from EPT1 to EPT2 cells. Our findings provide a novel stepwise cell culture model in which EMT emerges independently of transformation and is associated with subsequent accumulation of malignant features in prostate cells. Reprogramming of cell junction modules is
More>>
Ke, Xi-song;
[1]
Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)];
Li, Wen-cheng;
[1]
Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)];
Hovland, Randi;
[2]
Department of Molecular Biology, University of Bergen, Bergen (Norway)];
Qu, Yi;
[1]
Liu, Run-hui;
[3]
McCormack, Emmet;
[4]
Thorsen, Frits;
[5]
Olsen, Jan Roger;
[1]
Molven, Anders;
[1]
Department of Pathology, Haukeland University Hospital, Bergen (Norway)];
Kogan-Sakin, Ira;
Rotter, Varda;
[6]
Akslen, Lars A.;
[1]
Department of Pathology, Haukeland University Hospital, Bergen (Norway)];
Oyan, Anne Margrete;
[1]
Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)];
Kalland, Karl-Henning;
[1]
Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)]
- The Gade Institute, University of Bergen, Bergen (Norway)
- Center of Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen (Norway)
- Modern Research Center for Traditional Chinese Medicine, Second Military Medical University, Shanghai (China)
- Department of Medicine, Haukeland University Hospital, Bergen (Norway)
- Department of Biomedicine, University of Bergen, Bergen (Norway)
- Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot (Israel)
Citation Formats
Ke, Xi-song, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Li, Wen-cheng, Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)], Hovland, Randi, Department of Molecular Biology, University of Bergen, Bergen (Norway)], Qu, Yi, Liu, Run-hui, McCormack, Emmet, Thorsen, Frits, Olsen, Jan Roger, Molven, Anders, Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Kogan-Sakin, Ira, Rotter, Varda, Akslen, Lars A., Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Oyan, Anne Margrete, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Kalland, Karl-Henning, and Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)].
Reprogramming of cell junction modules during stepwise epithelial to mesenchymal transition and accumulation of malignant features in vitro in a prostate cell model.
United States: N. p.,
2011.
Web.
doi:10.1016/J.YEXCR.2010.10.009.
Ke, Xi-song, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Li, Wen-cheng, Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)], Hovland, Randi, Department of Molecular Biology, University of Bergen, Bergen (Norway)], Qu, Yi, Liu, Run-hui, McCormack, Emmet, Thorsen, Frits, Olsen, Jan Roger, Molven, Anders, Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Kogan-Sakin, Ira, Rotter, Varda, Akslen, Lars A., Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Oyan, Anne Margrete, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Kalland, Karl-Henning, & Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)].
Reprogramming of cell junction modules during stepwise epithelial to mesenchymal transition and accumulation of malignant features in vitro in a prostate cell model.
United States.
https://doi.org/10.1016/J.YEXCR.2010.10.009
Ke, Xi-song, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Li, Wen-cheng, Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)], Hovland, Randi, Department of Molecular Biology, University of Bergen, Bergen (Norway)], Qu, Yi, Liu, Run-hui, McCormack, Emmet, Thorsen, Frits, Olsen, Jan Roger, Molven, Anders, Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Kogan-Sakin, Ira, Rotter, Varda, Akslen, Lars A., Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Oyan, Anne Margrete, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Kalland, Karl-Henning, and Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)].
2011.
"Reprogramming of cell junction modules during stepwise epithelial to mesenchymal transition and accumulation of malignant features in vitro in a prostate cell model."
United States.
https://doi.org/10.1016/J.YEXCR.2010.10.009.
@misc{etde_22212087,
title = {Reprogramming of cell junction modules during stepwise epithelial to mesenchymal transition and accumulation of malignant features in vitro in a prostate cell model}
author = {Ke, Xi-song, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Li, Wen-cheng, Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)], Hovland, Randi, Department of Molecular Biology, University of Bergen, Bergen (Norway)], Qu, Yi, Liu, Run-hui, McCormack, Emmet, Thorsen, Frits, Olsen, Jan Roger, Molven, Anders, Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Kogan-Sakin, Ira, Rotter, Varda, Akslen, Lars A., Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Oyan, Anne Margrete, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Kalland, Karl-Henning, and Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)]}
abstractNote = {Epithelial to mesenchymal transition (EMT) is pivotal in tumor metastasis. 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. To promote prostate cell transformation, cells were maintained in saturation density cultures to select for cells overriding quiescence. Foci formed repeatedly following around 8 weeks in confluent EPT1 monolayers. Only later passage EPT1, but not EP156T cells of any passage, could form foci. Cells isolated from the foci were named EPT2 and formed robust colonies in soft agar, a malignant feature present neither in EP156T nor in EPT1 cells. EPT2 cells showed additional malignant traits in vitro, including higher ability to proliferate following confluence, higher resistance to apoptosis and lower dependence on exogenous growth factors than EP156T and EPT1 cells. Microarray profiling identified gene sets, many of which belong to cell junction modules, that changed expression from EP156T to EPT1 cells and continued to change from EPT1 to EPT2 cells. Our findings provide a novel stepwise cell culture model in which EMT emerges independently of transformation and is associated with subsequent accumulation of malignant features in prostate cells. Reprogramming of cell junction modules is involved in both steps.}
doi = {10.1016/J.YEXCR.2010.10.009}
journal = []
issue = {2}
volume = {317}
journal type = {AC}
place = {United States}
year = {2011}
month = {Jan}
}
title = {Reprogramming of cell junction modules during stepwise epithelial to mesenchymal transition and accumulation of malignant features in vitro in a prostate cell model}
author = {Ke, Xi-song, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Li, Wen-cheng, Urological Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022 (China)], Hovland, Randi, Department of Molecular Biology, University of Bergen, Bergen (Norway)], Qu, Yi, Liu, Run-hui, McCormack, Emmet, Thorsen, Frits, Olsen, Jan Roger, Molven, Anders, Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Kogan-Sakin, Ira, Rotter, Varda, Akslen, Lars A., Department of Pathology, Haukeland University Hospital, Bergen (Norway)], Oyan, Anne Margrete, Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)], Kalland, Karl-Henning, and Department of Microbiology, Haukeland, University Hospital, Bergen (Norway)]}
abstractNote = {Epithelial to mesenchymal transition (EMT) is pivotal in tumor metastasis. 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. To promote prostate cell transformation, cells were maintained in saturation density cultures to select for cells overriding quiescence. Foci formed repeatedly following around 8 weeks in confluent EPT1 monolayers. Only later passage EPT1, but not EP156T cells of any passage, could form foci. Cells isolated from the foci were named EPT2 and formed robust colonies in soft agar, a malignant feature present neither in EP156T nor in EPT1 cells. EPT2 cells showed additional malignant traits in vitro, including higher ability to proliferate following confluence, higher resistance to apoptosis and lower dependence on exogenous growth factors than EP156T and EPT1 cells. Microarray profiling identified gene sets, many of which belong to cell junction modules, that changed expression from EP156T to EPT1 cells and continued to change from EPT1 to EPT2 cells. Our findings provide a novel stepwise cell culture model in which EMT emerges independently of transformation and is associated with subsequent accumulation of malignant features in prostate cells. Reprogramming of cell junction modules is involved in both steps.}
doi = {10.1016/J.YEXCR.2010.10.009}
journal = []
issue = {2}
volume = {317}
journal type = {AC}
place = {United States}
year = {2011}
month = {Jan}
}