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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 389, Issue 6

Issues

Kallikrein 6 is a mediator of K-RAS-dependent migration of colon carcinoma cells

Rebecca S. Henkhaus
  • 1Cancer Biology Interdisciplinary Program, Arizona Cancer Center, The University of Arizona, 1515 N. Campbell Ave., Tucson, AZ 85724, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Eugene W. Gerner
  • 2Department of Biochemistry and Molecular Biophysics, Arizona Cancer Center, The University of Arizona, 1515 N. Campbell Ave., Tucson, AZ 85724, USA and Department of Cell Biology and Anatomy, Arizona Cancer Center, The University of Arizona, 1515 N. Campbell Ave., Tucson, AZ 85724, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Natalia A. Ignatenko
  • 3Department of Cell Biology and Anatomy, Arizona Cancer Center, The University of Arizona, 1515 N. Campbell Ave., Tucson, AZ 85724, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2008-05-15 | DOI: https://doi.org/10.1515/BC.2008.087

Abstract

Kallikrein 6 (KLK6) is a trypsin-like serine peptidase whose relevance in various types of cancers is currently being explored. Previous studies have shown that KLK6 mRNA is upregulated in colon and gastric cancers; however, the regulatory mechanisms and phenotypic consequences of this upregulation are largely unknown. Activating K-RAS mutations are common in colon cancer, occurring in approximately 50% of cases. We have recently reported the upregulation of KLK6 mRNA in Caco2 human colon cancer cells stably transfected with a mutant K-RAS allele (K-RASG12V). In this study we examined the pattern of K-RAS-dependent KLK6 expression and secretion in colon cancer cells. Using pharmacological inhibitors of pathways downstream of K-RAS, we could show that the PI3K and p42/44 MAPK pathways play an important role in the induction of KLK6 in mutant K-RAS-expressing colon cancer cells. Increased KLK6 expression enhanced colon cancer cell migration through laminin and Matrigel. Inhibition of KLK6 using small interference RNA treatment or a specific KLK6 antibody in Caco2 cells stably expressing the mutant K-RAS and in SW480 cells carrying a mutation in the K-RAS oncogene resulted in a reduction in invasiveness through cell culture inserts. These data support the oncogenic role of KLK6 in colorectal cancer.

Keywords: cell migration; colon cancer; kallikrein 6; K-Ras oncogene; Matrigel invasion

About the article

Corresponding author


Received: 2007-12-27

Accepted: 2008-02-15

Published Online: 2008-05-15

Published in Print: 2008-06-01


Citation Information: Biological Chemistry, Volume 389, Issue 6, Pages 757–764, ISSN (Online) 14374315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2008.087.

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