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Constitutive JAK/STAT3 Overexpression by Pancreatic Cancer is Inhibited by Pterostilbene In Vitro
*Denise McCormack1, *Debbie McDonald2, David McFadden2
1University of Vermont Department of Surgery, Danbury Hospital Department of Surgery, Burlington, VT;2University of Vermont Department of Surgery, Burlington, VT
Objective: To examine the influence of pterostilbene upon JAK/STAT3, an essential transcription pathway in pancreatic carcinogenesis and metastasis.
Design: In vitro pancreatic cancer JAK/STAT3 inhibition model
Setting: Basic science laboratory
Interventions: The pancreatic cancer cell lines MIA and PANC-1 were cultured in media and allowed to adhere overnight. Cells were incubated with concentrations of 25 and 50 micromolar pterostilbene for 24 and 48 hours. Control samples were incubated with media alone. Detection of phosphorylated STAT3 was performed using a sandwich ELISA protocol.
Main Outcome Measures: STAT3 phosphorylation in untreated and pterostilbene-treated pancreatic cancer cells.
Results: Pterostilbene treatment inhibited STAT3 phosphorylation in a dose-dependent manner (p < 0.01). Additionally, in both cell lines, pterostilbene inhibited STAT3 phosphorylation in a time-dependent manner (p < 0.01).
Conclusions: We have recently demonstrated that pterostilbene (3, 5- dimethoxy-4-hydroxystilbene), an anti-oxidant found in blueberries, inhibits pancreatic cancer growth in vitro and in vivo. This study’s aim was to evaluate the mechanism of pterostilbene’s profound antiproliferative effects. The JAK/STAT3 pathway is a critical component of pancreatic tumorigenesis and metastasis. Previous studies have shown that many pancreatic cancers overexpress phosphorylated STAT3, leading to constitutive JAK/STAT3 signaling and unchecked cell growth. We have now demonstrated that pterostilbene inhibits pancreatic cancer growth in vitro by downregulation of JAK/STAT3 signaling. This effect is both time and dose dependent. Further studies are ongoing to define the adjuvant role of pterostilbene against pancreatic cancer.
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Abstract Submission Deadline:
May 5, 2014
August 13, 2014
Early Bird Registration Deadline:
August 11, 2014