Replacement of Fhit in cancer cells suppresses tumorigenicity.
basic_science · Level V
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- Record sourced from PubMed, PMID 9391102.
- Also identified by PMC identifier 28382.
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Abstract
The candidate tumor suppressor gene, FHIT, encompasses the common human chromosomal fragile site at 3p14.2, the hereditary renal cancer translocation breakpoint, and cancer cell homozygous deletions. Fhit hydrolyzes dinucleotide 5',5"'-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',5"'-P1, P3-triphosphate hydrolysis is not required for tumor suppression.
Medical subject headings
- Acid Anhydride Hydrolases
- Genes, Tumor Suppressor
- Neoplasm Proteins
- Proteins