Open Accessp53 functions as a cell cycle control protein in osteosarcomas.
Author(s) -
Lisa Diller,
Jayne Kassel,
Camille E. Nelson,
Magdalena A. Gryka,
G Litwak,
Mark C. Gebhardt,
Brigitte Bressac,
Mehmet Öztürk,
Suzanne J. Baker,
Bert Vogelstein
Publication year - 1990
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.10.11.5772
Subject(s) - biology , gene , transfection , osteosarcoma , cell cycle , point mutation , saccharomyces cerevisiae , cell cycle checkpoint , cell growth , cell cycle protein , mutation , cancer research , genetics , microbiology and biotechnology
Mutations in the p53 gene have been associated with a wide range of human tumors, including osteosarcomas. Although it has been shown that wild-type p53 can block the ability of E1a and ras to cotransform primary rodent cells, it is poorly understood why inactivation of the p53 gene is important for tumor formation. We show that overexpression of the gene encoding wild-type p53 blocks the growth of osteosarcoma cells. The growth arrest was determined to be due to an inability of the transfected cells to progress into S phase. This suggests that the role of the p53 gene as an antioncogene may be in controlling the cell cycle in a fashion analogous to the check-point control genes in Saccharomyces cerevisiae.