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[Cancer Research 63, 882-886, February 15, 2003]
© 2003 American Association for Cancer Research

Tumor Biology

An Adenovirus Carrying the Rat Protein Tyrosine Phosphatase {eta} Suppresses the Growth of Human Thyroid Carcinoma Cell Lines in Vitro and in Vivo1

Rodolfo Iuliano, Francesco Trapasso, Ilaria Le Pera, Filippo Schepis, Irene Samà, Alessandra Clodomiro, Kristoffel R. Dumon, Massimo Santoro, Lorenzo Chiariotti, Giuseppe Viglietto and Alfredo Fusco2

Dipartimento di Medicina Sperimentale e Clinica, Facoltà di Medicina e Chirurgia di Catanzaro, Università degli Studi di Catanzaro "Magna Graecia," 88100 Catanzaro, Italy [R. I., F. T., I. L. P., F. S., I. S., A. C., L. C., A. F.]; Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107 [K. R. D.]; and Centro di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia, Università di Napoli "Federico II," 80131 Napoli, Italy [M. S., G. V., A. F.]

We demonstrated previously that rat tyrosine phosphatase r-PTP{eta} expression was suppressed in rat and human thyroid neoplastic cells, and that restoration of r-PTP{eta} expression reverted the malignant phenotype. To investigate the potential of this gene for cancer therapy, we generated an adenovirus carrying the r-PTP{eta} cDNA (Ad-r-PTP{eta}). This virus infected human thyroid carcinoma cells and overexpressed the r-PTP{eta} protein. Overexpression of r-PTP{eta} significantly inhibited the growth of four thyroid carcinoma cell lines. Cell growth inhibition was associated with down-regulation of extracellular signal-regulated kinase 1/2 activity, with increased levels of the cell-cycle inhibitor p27kip1 protein and with dephosphorylation of PLC{gamma}1, a substrate of DEP-1, the human homologue of r-PTP{eta}. Finally, the growth of xenograft tumors induced in athymic mice by anaplastic thyroid carcinoma ARO cells transduced with the Ad-r-PTP{eta} virus was drastically reduced. These data suggest that gene therapy based on restoration of PTP{eta} function has potential in the treatment of human thyroid malignant neoplasias.




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