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Suppression of human colorectal carcinoma cell growth by wild-type p53.

Mutations of the p53 gene occur commonly in colorectal carcinomas and the wild-type p53 allele is often concomitantly deleted. These findings suggest that the wild-type gene may act as a suppressor of colorectal carcinoma cell growth. To test this hypothesis, wild-type or mutant human p53 genes were transfected into human colorectal carcinoma cell lines. Cells transfected with the wild-type gene formed colonies five- to tenfold less efficiently than those transfected with a mutant p53 gene. In those colonies that did form after wild-type gene transfection, the p53 sequences were found to be deleted or rearranged, or both, and no exogenous p53 messenger RNA expression was observed. In contrast, transfection with the wild-type gene had no apparent effect on the growth of epithelial cells derived from a benign colorectal tumor that had only wild-type p53 alleles. Immunocytochemical techniques demonstrated that carcinoma cells expressing the wild-type gene did not progress through the cell cycle, as evidenced by their failure to incorporate thymidine into DNA. These studies show that the wild-type gene can specifically suppress the growth of human colorectal carcinoma cells in vitro and that an in vivo-derived mutation resulting in a single conservative amino acid substitution in the p53 gene product abrogates this suppressive ability.

Pubmed ID: 2144057

Authors

  • Baker SJ
  • Markowitz S
  • Fearon ER
  • Willson JK
  • Vogelstein B

Journal

Science (New York, N.Y.)

Publication Data

August 24, 1990

Associated Grants

  • Agency: NCI NIH HHS, Id: CA 43703
  • Agency: NIGMS NIH HHS, Id: GM 07184
  • Agency: NIGMS NIH HHS, Id: GM 07309

Mesh Terms

  • Cell Division
  • Cell Line
  • Colonic Neoplasms
  • DNA Replication
  • Humans
  • Nuclear Proteins
  • Oncogene Proteins
  • Phosphoproteins
  • Plasmids
  • RNA, Messenger
  • Rectal Neoplasms
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53