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Molecular Cancer Research
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CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP

Wei Jiang, Yaqing Zhang, Kevin T. Kane, Meredith A. Collins, Diane M. Simeone, Marina Pasca di Magliano and Kevin Tri Nguyen
Wei Jiang
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
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Yaqing Zhang
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
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Kevin T. Kane
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
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Meredith A. Collins
2Program in Cell and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan.
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Diane M. Simeone
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
3Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan.
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Marina Pasca di Magliano
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
2Program in Cell and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan.
4Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan.
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  • For correspondence: marinapa@umich.edu ktnguyen74@yahoo.com
Kevin Tri Nguyen
1Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
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  • For correspondence: marinapa@umich.edu ktnguyen74@yahoo.com
DOI: 10.1158/1541-7786.MCR-14-0076 Published January 2015
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Abstract

Pancreatic cancer is one of the deadliest human malignancies due to its early metastatic spread and resistance to therapy. The mechanisms regulating pancreatic cancer metastasis are so far poorly understood. Here, using both in vitro and in vivo approaches, it is demonstrated that CD44, a transmembrane glycoprotein expressed on a subset of pancreatic cancer cells, is required for the induction of epithelial–mesenchymal transition (EMT) and the activation of an invasive program in pancreatic cancer. Mechanistically, the transcription factor Snail1 (SNAI1), a regulator of the EMT program, is a downstream target of CD44 in primary pancreatic cancer cells and regulates membrane bound metalloproteinase (MMP14/MT1-MMP) expression. In turn, MT1-MMP expression is required for pancreatic cancer invasion. Thus, these data establish the CD44–Snail–MMP axis as a key regulator of the EMT program and of invasion in pancreatic cancer.

Implications: This study sets the stage for CD44 and MT1-MMP as therapeutic targets in pancreatic cancer, for which small molecule or biologic inhibitors are available.

Visual Overview: http://mcr.aacrjournals.org/content/early/2014/09/10/1541-7786.MCR-14-0076/F1.large.jpg.

Mol Cancer Res; 13(1); 9–15. ©2014 AACR.

Footnotes

  • Note: Supplementary data for this article are available at Molecular Cancer Research Online (http://mcr.aacrjournals.org/).

  • Received February 12, 2014.
  • Revision received August 18, 2014.
  • Accepted August 20, 2014.
  • ©2014 American Association for Cancer Research.
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Molecular Cancer Research: 13 (1)
January 2015
Volume 13, Issue 1
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CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Wei Jiang, Yaqing Zhang, Kevin T. Kane, Meredith A. Collins, Diane M. Simeone, Marina Pasca di Magliano and Kevin Tri Nguyen
Mol Cancer Res January 1 2015 (13) (1) 9-15; DOI: 10.1158/1541-7786.MCR-14-0076

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CD44 Regulates Pancreatic Cancer Invasion through MT1-MMP
Wei Jiang, Yaqing Zhang, Kevin T. Kane, Meredith A. Collins, Diane M. Simeone, Marina Pasca di Magliano and Kevin Tri Nguyen
Mol Cancer Res January 1 2015 (13) (1) 9-15; DOI: 10.1158/1541-7786.MCR-14-0076
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