gms | German Medical Science

128. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

03.05. - 06.05.2011, München

Lipocalin-2 expression in human colon cancer is associated with synchronous metastasis and poor survival

Meeting Abstract

  • Herbert T. Maier - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Birgit Trenkwalder - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Matthias Zitt - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Hubert Schwelberger - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Felix Aigner - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Alexander Perathoner - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Patricia Moser - Universitätsklinik Insbruck, Abteilung für Pathologie, Innsbruck
  • Jakob Troppmair - Universitätsklinik Innsbruck, Daniel Swarovski Forschungslabor, Innsbruck
  • Dietmar Öfner-Velano - Paracelsus Medizinische Privatuniversität Salzburg, Universitätsklinik für Chirurgie, Salzburg
  • Raimund Margreiter - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Albert Amberger - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck
  • Johann Pratschke - Universitätsklinik Innsbruck, Abteilung für Viszeral-, Thorax- und Transplantationschirurgie, Innsbruck

Deutsche Gesellschaft für Chirurgie. 128. Kongress der Deutschen Gesellschaft für Chirurgie. München, 03.-06.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11dgch305

DOI: 10.3205/11dgch305, URN: urn:nbn:de:0183-11dgch3054

Published: May 20, 2011

© 2011 Maier et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Introduction: Lipocalin-2 was recently shown to be highly expressed in various human cancers and increased protein levels were associated with worse survival of patients with breast, gastric or oesophageal cancer. The main focus of this work was to analyze the possible implication of Lcn-2 upregulation in colon cancer development.

Materials and methods: Expression of Lcn-2 was analyzed in various colorectal carcinoma cell lines, paired colorectal carcinoma tissues and normal mucosas by Western blot. Lcn-2 immunostaining was performed in 213 colorectal carcinoma resection specimens and correlated with clinical parameters. Colorectal carcinoma cell lines were treated with various concentrations of recombinant Lcn-2 protein and monitored for growth and survival.

Results: Western blot analysis of colorectal carcinoma cell lines and tissues clearly demonstrated Lcn-2 overexpression in carcinomas. Immunostaining revealed Lcn-2 overexpression in 199 (93,4%) of colorectal carcinoma tissues. Intense immunoreactivity was significantly correlated with synchronous metastases (p<0,03), UICC stage (p<0,02) and tumor grading (p<0,009). Cancer samples of the right hemicolon showed significantly higher Lcn-2 expression decreasing in the left hemicolon and the rectum (p<0,001). Addition of various concentrations of recombinant human Lcn-2 protein to carcinoma cell lines did not have any influence on cell growth and survival in vitro.

Conclusion: Our data provide evidence that Lcn-2 expression is upregulated with tumor progression. The correlation of Lcn-2 expression with localisation in the colon gives molecular biological evidence for distinguishing subsites of colorectal cancer. Targeting Lcn-2 might be a new therapeutic strategy in colorectal carcinoma.