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Carcinogenesis Advance Access originally published online on July 1, 2004
Carcinogenesis 2004 25(11):2107-2114; doi:10.1093/carcin/bgh224
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Carcinogenesis vol.25 no.11 © Oxford University Press 2004; all rights reserved.

ARTICLE

Restoration of receptor-type protein tyrosine phosphatase {eta} function inhibits human pancreatic carcinoma cell growth in vitro and in vivo

Francesco Trapasso1,2, Sai Yendamuri1, Kristoffel R. Dumon1, Rodolfo Iuliano2, Rossano Cesari1, Byron Feig1, Robin Seto1, Luisa Infante1, Hideshi Ishii1, Andrea Vecchione1, Matthew J. During3, Carlo M. Croce1 and Alfredo Fusco4,5

1 Kimmel Cancer Institute, Thomas Jefferson University, 233S 10th Street, Philadelphia, PA 19107, USA, 2 Dipartimento di Medicina Sperimentale e Clinica, Università ‘Magna Græcia’, via T. Campanella, 5, I-88100 Catanzaro, Italy, 3 Department of Neurosurgery, CNS Gene Therapy Center, Thomas Jefferson University, 1025 Walnut Street, Philadelphia, PA 19107, USA and 4 Centro di Endocrinologia ed Oncologia Sperimentale del C.N.R. c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli ‘Federico II’, via Pansini, 5, I-80131 Naples, Italy

5 To whom correspondence should be addressed Email: afusco{at}napoli.com

DEP-1/HPTP{eta}, a receptor-type protein tyrosine phosphatase, is a candidate tumor suppressor gene because its expression was blocked in rat and human thyroid transformed cells, and its restoration reverted their neoplastic phenotype. In addition, loss of DEP-1/HPTP{eta} heterozygosity has been described in mammary, lung and colon primary tumors. We now show that DEP-1/HPTP{eta} is drastically reduced in several cell lines originating from human epithelial pancreatic carcinomas compared with normal pancreatic tissue. We also show that the infection of AsPC1 and PSN1 cells with a recombinant adenovirus carrying r-PTP{eta} cDNA (the rat homolog of DEP-1/HPTP{eta}) inhibits their proliferation. Flow cytometric analysis of the infected cells demonstrated that restoration of r-PTP{eta} activity disrupts their cell cycle and leads to apoptosis. Finally, the growth of PSN1 xenograft tumors was blocked by the intratumoral injection of a recombinant adeno-associated virus carrying r-PTP{eta}. The data suggest that restoration of DEP-1/HPTP{eta} expression could be a useful tool for the gene therapy of human pancreatic cancers.


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