Search

Your search keyword '"Trapasso, F"' showing total 3 results
Start Over Author "Trapasso, F" Journal carcinogenesis
3 results on '"Trapasso, F"'

2. Restoration of receptor-type protein tyrosine phosphatase function inhibits human pancreatic carcinoma cell growth in vitro and in vivo

Author

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

Subjects
Cancer Research, Pancreatic disease, Genotype, tumor suppressor, Protein tyrosine phosphatase, Biology, Transfection, Polymerase Chain Reaction, Cell Line, Tumor, Pancreatic cancer, human pancreatic carcinoma cell, medicine, Animals, Humans, Genes, Tumor Suppressor, DNA Primers, DEP-1/HPTPeta, Reverse Transcriptase Polymerase Chain Reaction, Cell growth, Receptor-Like Protein Tyrosine Phosphatases, Class 3, Exons, General Medicine, Cell cycle, medicine.disease, Candidate Tumor Suppressor Gene, Rats, Pancreatic Neoplasms, Kinetics, medicine.anatomical_structure, Cell culture, Cancer research, Protein Tyrosine Phosphatases, Pancreas, Cell Division
Abstract

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

Published
2004

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

Author

Trapasso F, Yendamuri S, Dumon KR, Iuliano R, Cesari R, Feig B, Seto R, Infante L, Ishii H, Vecchione A, During MJ, Croce CM, and Fusco A

Subjects
Animals, Cell Division, Cell Line, Tumor, DNA Primers, Exons genetics, Genotype, Humans, Kinetics, Pancreatic Neoplasms genetics, Polymerase Chain Reaction, Rats, Receptor-Like Protein Tyrosine Phosphatases, Class 3, Reverse Transcriptase Polymerase Chain Reaction, Transfection, Genes, Tumor Suppressor, Pancreatic Neoplasms enzymology, Pancreatic Neoplasms pathology, Protein Tyrosine Phosphatases genetics, Protein Tyrosine Phosphatases metabolism
Abstract

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

Published
2004
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results