Journal
CANCER CELL
Volume 19, Issue 4, Pages 441-455Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2011.03.002
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Funding
- UCSF Diabetes and Endocrinology Research Center
- Pancreatic Cancer Action Network
- NIH [CA112537, R03 CA115225, P30CA042014]
- Japan Society for the Promotion of Science
- Klein Family Foundation
- National Pancreas Foundation
- NIH, National Cancer Institute [F32]
- American College of Surgeons Resident Research
- Huntsman Cancer Institute
- Huntsman Cancer Foundation
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Chronic pancreatitis is a well-known risk factor for pancreatic ductal adenocarcinoma (PDA) development in humans, and inflammation promotes PDA initiation and progression in mouse models of the disease. However, the mechanistic link between inflammatory damage and PDA initiation is unclear. Using a Kras-driven mouse model of PDA, we establish that the inflammatory mediator Stat3 is a critical component of spontaneous and pancreatitis-accelerated PDA precursor formation and supports cell proliferation, metaplasia-associated inflammation, and MMP7 expression during neoplastic development. Furthermore, we show that Stat3 signaling enforces MMP7 expression in PDA cells and that MMP7 deletion limits tumor size and metastasis in mice. Finally, we demonstrate that serum MMP7 level in human patients with PDA correlated with metastatic disease and survival.
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