| Prevention and delay in progression of human pancreatic cancer by stable overexpression of the opioid growth factor receptor |
Authors: Ian S. Zagon, Shawn Kreiner, Jeffery J. Heslop, Andrea B. Conway, Clinton R. Morgan, Patricia J. McLaughlin |
Affiliations:
Department of Neural and Behavioral Sciences, H109, The M.S. Hershey Medical Center, Hershey, PA 17033, USA. isz1@psu.edu
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Doi: 10.3892/ijo_00000011 |
Pages: 317-323 |
Abstract:
This study examined overexpression of the opioid growth factor receptor (OGFr) in pancreatic cancer cells and phenotypic changes in tumorigenicity. Tumors of MIA PaCa-2 cells transfected with OGFr cDNA (OGFr-1) had 3.3 times more OGFr than empty vector (EV) neoplasias, and 4.3 times more OGFr than tumors from wild-type (WT) mice. No differences in OGFr binding were detected between tumors of EV and WT animals. Tumor incidence in OGFr-1 animals was reduced by up to 50% from EV mice. Latency times for OGFr-1 tumor expression were increased 30%, tumor volume was decreased 70%, and DNA synthesis was reduced 24% relative to EV mice. Exogenous OGF reduced OGFr-1 tumor volume up to 55% compared to OGFr-1 mice given vehicle. These data support OGFr gene function as a regulator of cell proliferation that impacts on tumorigenic expression, and suggest that molecular and pharmacological manipulation of OGFr may prevent or delay human pancreatic cancer.
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