Journal Article

Restoration of receptor-type protein tyrosine phosphatase η function inhibits human pancreatic carcinoma cell growth <i>in vitro</i> and <i>in vivo</i>

Francesco Trapasso, Sai Yendamuri, Kristoffel R. Dumon, Rodolfo Iuliano, Rossano Cesari, Byron Feig, Robin Seto, Luisa Infante, Hideshi Ishii, Andrea Vecchione, Matthew J. During, Carlo M. Croce and Alfredo Fusco

in Carcinogenesis

Volume 25, issue 11, pages 2107-2114
Published in print November 2004 | ISSN: 0143-3334
Published online November 2004 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgh224
Restoration of receptor-type protein tyrosine phosphatase η function inhibits human pancreatic carcinoma cell growth in vitro and in vivo

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DEP-1/HPTPη, 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/HPTPη heterozygosity has been described in mammary, lung and colon primary tumors. We now show that DEP-1/HPTPη 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-PTPη cDNA (the rat homolog of DEP-1/HPTPη) inhibits their proliferation. Flow cytometric analysis of the infected cells demonstrated that restoration of r-PTPη 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-PTPη. The data suggest that restoration of DEP-1/HPTPη expression could be a useful tool for the gene therapy of human pancreatic cancers.

Keywords: AAV, adeno-associated virus; MOI, multiplicity of infection; TUNEL, terminal deoxynucleotidyl transferase mediated X-dUTP nick end labeling; VP, viral particles.

Journal Article.  5834 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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