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P-cadherin in adhesion and invasion: opposite roles in colon and bladder carcinoma

Veerle Van Marck UGent, Christophe Stove UGent, Koen Jacobs UGent, Gert Van den Eynden and Marc Bracke UGent (2011) INTERNATIONAL JOURNAL OF CANCER. 128(5). p.1031-1044
abstract
Neoexpression or upregulation of placental cadherin (P-cadherin), a member of the classical cadherin family, has previously been described in several carcinomas, such as colorectal and bladder carcinomas. In this study, we combined two different approaches, immunohistochemistry of tumor samples and in vitro knockdown of P-cadherin, to gain a better insight into the role of P-cadherin in these types of cancer. First, we performed immunohistochemistry for P- and E-cadherins in a series of 52 colorectal adenocarcinomas, including well, moderately and poorly differentiated (WD, MD, and PD) tumors. Decrease or loss of P-cadherin neoexpression was significantly associated with a higher tumor grade and could discriminate WD from MD and/or PD tumors (p < 0.001). E-cadherin, on the other hand, was strongly expressed at the membrane of most WD (18 of 19) and MD tumors (15 of 19). Downregulation correlated significantly with the PD phenotype (p < 0.001). In a second approach, we transiently or stably knocked down P-cadherin in HT-29 colon adenocarcinoma cells. This led to decreased intercellular adhesion and to an increased migratory and long-term invasive phenotype compared with control HT-29 cells, suggesting that P-cadherin acts as a proadhesive and anti-invasive/antimigratory molecule in colon carcinoma cells. Contrasting with these results and illustrating the context-specific function of P-cadherin were our results obtained in RT-112 bladder carcinoma cells. Stable knockdown of P-cadherin in RT-112 cells diminished invasion and migration, and promoted intercellular adhesion.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
invasion, bladder cancer, P-cadherin, adhesion, colorectal cancer, TRANSITIONAL-CELL-CARCINOMA, BREAST-CANCER CELLS, N-CADHERIN, COLORECTAL-CANCER, CATENIN EXPRESSION, PROGNOSTIC-SIGNIFICANCE, MESENCHYMAL TRANSITION, NEOPLASTIC PROGRESSION, GASTRIC CARCINOMAS, GROWTH-FACTOR
journal title
INTERNATIONAL JOURNAL OF CANCER
Int. J. Cancer
volume
128
issue
5
pages
1031 - 1044
Web of Science type
Article
Web of Science id
000286960300004
JCR category
ONCOLOGY
JCR impact factor
5.444 (2011)
JCR rank
26/190 (2011)
JCR quartile
1 (2011)
ISSN
0020-7136
DOI
10.1002/ijc.25427
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1035686
handle
http://hdl.handle.net/1854/LU-1035686
date created
2010-09-01 16:07:34
date last changed
2012-04-26 11:18:07
@article{1035686,
  abstract     = {Neoexpression or upregulation of placental cadherin (P-cadherin), a member of the classical cadherin family, has previously been described in several carcinomas, such as colorectal and bladder carcinomas. In this study, we combined two different approaches, immunohistochemistry of tumor samples and in vitro knockdown of P-cadherin, to gain a better insight into the role of P-cadherin in these types of cancer. First, we performed immunohistochemistry for P- and E-cadherins in a series of 52 colorectal adenocarcinomas, including well, moderately and poorly differentiated (WD, MD, and PD) tumors. Decrease or loss of P-cadherin neoexpression was significantly associated with a higher tumor grade and could discriminate WD from MD and/or PD tumors (p {\textlangle} 0.001). E-cadherin, on the other hand, was strongly expressed at the membrane of most WD (18 of 19) and MD tumors (15 of 19). Downregulation correlated significantly with the PD phenotype (p {\textlangle} 0.001). In a second approach, we transiently or stably knocked down P-cadherin in HT-29 colon adenocarcinoma cells. This led to decreased intercellular adhesion and to an increased migratory and long-term invasive phenotype compared with control HT-29 cells, suggesting that P-cadherin acts as a proadhesive and anti-invasive/antimigratory molecule in colon carcinoma cells. Contrasting with these results and illustrating the context-specific function of P-cadherin were our results obtained in RT-112 bladder carcinoma cells. Stable knockdown of P-cadherin in RT-112 cells diminished invasion and migration, and promoted intercellular adhesion.},
  author       = {Van Marck, Veerle and Stove, Christophe and Jacobs, Koen and Van den Eynden, Gert and Bracke, Marc},
  issn         = {0020-7136},
  journal      = {INTERNATIONAL JOURNAL OF CANCER},
  keyword      = {invasion,bladder cancer,P-cadherin,adhesion,colorectal cancer,TRANSITIONAL-CELL-CARCINOMA,BREAST-CANCER CELLS,N-CADHERIN,COLORECTAL-CANCER,CATENIN EXPRESSION,PROGNOSTIC-SIGNIFICANCE,MESENCHYMAL TRANSITION,NEOPLASTIC PROGRESSION,GASTRIC CARCINOMAS,GROWTH-FACTOR},
  language     = {eng},
  number       = {5},
  pages        = {1031--1044},
  title        = {P-cadherin in adhesion and invasion: opposite roles in colon and bladder carcinoma},
  url          = {http://dx.doi.org/10.1002/ijc.25427},
  volume       = {128},
  year         = {2011},
}

Chicago
Van Marck, Veerle, Christophe Stove, Koen Jacobs, Gert Van den Eynden, and Marc Bracke. 2011. “P-cadherin in Adhesion and Invasion: Opposite Roles in Colon and Bladder Carcinoma.” International Journal of Cancer 128 (5): 1031–1044.
APA
Van Marck, V., Stove, C., Jacobs, K., Van den Eynden, G., & Bracke, M. (2011). P-cadherin in adhesion and invasion: opposite roles in colon and bladder carcinoma. INTERNATIONAL JOURNAL OF CANCER, 128(5), 1031–1044.
Vancouver
1.
Van Marck V, Stove C, Jacobs K, Van den Eynden G, Bracke M. P-cadherin in adhesion and invasion: opposite roles in colon and bladder carcinoma. INTERNATIONAL JOURNAL OF CANCER. 2011;128(5):1031–44.
MLA
Van Marck, Veerle, Christophe Stove, Koen Jacobs, et al. “P-cadherin in Adhesion and Invasion: Opposite Roles in Colon and Bladder Carcinoma.” INTERNATIONAL JOURNAL OF CANCER 128.5 (2011): 1031–1044. Print.