Wild-type p53 suppresses growth of human prostate cancer cells containing mutant p53 alleles.
作者： William B. Isaacs , Bob S. Carter , Charles M. Ewing
DOI:
关键词: Molecular biology 、 Biology 、 Gene 、 Gene mutation 、 Carcinogenesis 、 Therapeutic gene modulation 、 PAX4 、 Cancer research 、 Chromoplexy 、 DU145 、 Mutant
摘要: Abstract Evidence supporting a broad role for the inactivation of p53 gene in human tumorigenesis has been provided by studies showing that is mutated many cancers. In this study, we report on mutational status prostate cancer cells and provide functional evidence wild-type may have suppressing prostatic tumorigenesis. Sequence analysis exons 5–8 reveals three five cell lines (TSUPr-1, PC3, DU145) contain mutations which alter amino acid sequence most highly conserved portion gene. One two primary specimens examined also contained mutation region. Transfection versus into with results reduced colony formation. Wild-type expression apparently incompatible continued growth these tumor inasmuch as none colonies formed after transfections retain transfected sequences. Immunocytochemical data indicate carcinoma expressing are arrested because they exhibit level thymidine incorporation DNA. This study first suggests
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