Date of Award
Restricted Access Thesis
Master of Science
Field of Study
Microbiology and Immunology
Graduate School of Biomedical Sciences
Johnson, C., The regulation of p53 by protein kinase C in anticancer drug-induced apoptosis. Master of Science (Microbiology and Immunology), December, 2001. 43 pp., 11 figures, references, 6 titles. The tumor suppression protein p53 has been implicated in DNA damage-induced apoptosis. Previous studies demonstrated that the protein kinase C (PKC) signal transduction pathway regulates apoptosis induced by the DNA damaging agent cisplatin and is deregulated in cisplatin-resistant cells. The present study examined whether PKC influences p53 and, hence, cellular sensitivity to cisplatin. Basal p53 levels were elevated in cisplatin-resistant HeLa (HeLa/CP) cells as compared to parental HeLa cells. Cisplatin further increased p53 levels in HeLA/CP, but not in HeLA cells. However, rottlerin, a PKC-δ inhibitor that prevents cisplatin-induced apoptosis, caused p53 accumulation in HeLa cells treated with cisplatin. Rottlerin stabilized p53 in response to cisplatin in HeLa cells, whereas cisplatin alone was sufficient to stabilize p53 in HeLa/CP cells.
Johnson, C. L.
"The Regulation of P53 by Protein Kinase C in Anticancer Drug-Induced Apoptosis" Fort Worth, Tx: University of North Texas Health Science Center;