| Literature DB >> 21186400 |
Gail L Matters1, Christopher McGovern, John F Harms, Kevin Markovic, Krystal Anson, Calpurnia Jayakumar, Melissa Martenis, Christina Awad, Jill P Smith.
Abstract
Cholecystokinin (CCK) and gastrin stimulate growth of pancreatic cancer. Although down-regulation of gastrin inhibits growth of pancreatic cancer, the contribution of endogenous CCK to tumor growth is unknown. The purpose of this study was to evaluate the role of endogenous CCK on autocrine growth of pancreatic cancer. Pancreatic cancer cell lines were analyzed for CCK mRNA and peptide expression by real-time RT-PCR and radioimmunoassay, respectively. The effect of endogenous CCK on growth was evaluated by treating cancer cells with CCK neutralizing antibodies and by down-regulating CCK mRNA by RNAi. Wild-type pancreatic cancer cells expressed significantly lower CCK mRNA and peptide levels than gastrin. Neither treatment of pancreatic cancer cells with CCK antibodies nor the down-regulation of CCK mRNA and peptide by shRNAs altered growth in vitro or in vivo. Conversely, when gastrin mRNA expression was down-regulated, the same cells failed to produce tumors in spite of having sustained levels of endogenous CCK. Pancreatic cancer cells produce CCK and gastrin; however, the autocrine production of gastrin is more important for stimulating tumor growth.Entities:
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Year: 2010 PMID： 21186400 PMCID： PMC3282828 DOI： 10.3892/ijo.2010.886
Source DB: PubMed Journal: Int J Oncol ISSN： 1019-6439 Impact factor: 5.650