Cholecystokinin Mediates Progression and Metastasis of Pancreatic Cancer Associated with Dietary Fat

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• 作者：Gail L. Matters (1)
  Timothy K. Cooper (2) (3)
  Christopher O. McGovern (4)
  Evan L. Gilius (4)
  Jiangang Liao (5)
  Brian M. Barth (6)
  Mark Kester (6)
  Jill P. Smith (4) (7)
  
• 关键词：Pancreatic cancer ; Devazepide ; Obesity ; High ; fat diet ; CCK ; Metastasis
• 刊名：Digestive Diseases and Sciences
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：59
• 期：6
• 页码：1180-1191
• 全文大小：
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• 作者单位：Gail L. Matters (1)
  Timothy K. Cooper (2) (3)
  Christopher O. McGovern (4)
  Evan L. Gilius (4)
  Jiangang Liao (5)
  Brian M. Barth (6)
  Mark Kester (6)
  Jill P. Smith (4) (7)
  
  1. Department of Biochemistry and Molecular Biology, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  2. Department of Comparative Medicine, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  3. Department of Pathology, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  4. Department of Medicine, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  5. Department of Public Health Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  6. Department of Pharmacology, College of Medicine, The Pennsylvania State University, Hershey, PA, 17033, USA
  7. Department of Medicine, Georgetown University Hospital, 3800 Reservoir Rd, NW, 2 Main, 2nd Floor, Washington, DC, 20007, USA
  
• ISSN：1573-2568

文摘

Background Obesity and dietary fat are associated with increased risk of several malignancies including pancreatic cancer. The incidence of pancreatic cancer is increased in countries that consume diets high in fat. Aim The purpose of this study was to assess the relationship and mechanism of action between dietary fat and endogenous cholecystokinin (CCK) on pancreatic tumor growth and metastasis in an immunocompetent animal model. Methods C57BL/6 mice were placed on regular, low-fat, or high-fat diets for 8?weeks before establishment of Panc-02 orthotopic pancreatic tumors. Mice were then treated with a CCK-A receptor antagonist, devazepide, or vehicle for an additional 2.5?weeks. Pancreas tumors were weighed and metastases counted. Blood CCK levels were measured by radioimmunoassay (RIA). Tissues were examined histologically and studied for genes associated with metastasis by RT-PCR array. Effects of the CCK antagonist on Panc-02 cells invasiveness was assessed in a Matrigel invasion assay. Results Mice that received the high-fat diet had larger tumors and tenfold higher serum CCK levels by RIA compared to normal diet controls (p?<?0.01). Pancreatic tumors in high-fat diet mice treated with the antagonist had fewer intravascular tumor emboli and metastases compared to controls. The reduction in tumor emboli correlated with decreased vascular endothelial growth factor-A (VEGF-A) expression in tumors (p?<?6?×?10?). In vitro invasiveness of Panc-02 cells also was reduced by CCK-A receptor antagonist treatment (p?=?1.33?×?10?). Conclusion CCK is a mediator of dietary fat-associated pancreatic cancer. CCK is also involved in the invasiveness of pancreatic tumors through a mechanism involving VEGF-A.