| Abstract: |
The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal caller translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5m-P1,P3-triphosphate in vitro and mutation of a central histidine abolishes hydrolase activity. To study Fhit function, wild-type and mutant FHIT genes were transfected into cancer cell lines that lacked endogenous Fhit. No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase 'dead' Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5m-P1,P3-triphosphate hydrolysis is not required for tumor suppression. |
| Keywords: |
mutation; nonhuman; proteins; animal cell; mouse; phenotype; animals; mice; cell division; gene expression; neoplasm proteins; tumor cells, cultured; acid anhydride hydrolases; transfection; animalia; mus musculus; cancer inhibition; tumor suppressor gene; genetic transfection; nude mouse; mice, nude; cancer cell; carcinogenicity; transplantation, heterologous; neoplasm transplantation; chromosome 3p; genes, tumor suppressor; gene structure; chromosomes, human, pair 3; dinucleoside phosphates; phosphoric diester hydrolases; hydrolase; chromosome fragility; humans; priority journal; article; chromosome fragile site; chromosome fragile sites
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