The Regulation of P53 by Protein Kinase C in Anticancer Drug-Induced Apoptosis
Abstract
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.
Subject
Cancer Biology
Cell and Developmental Biology
Cell Biology
Cells
Cellular and Molecular Physiology
Life Sciences
Medical Cell Biology
Medical Genetics
Medicine and Health Sciences
Other Cell and Developmental Biology
Basal P53
protein kinase C
anticancer-drug induced apoptosis
tumor suppression protein
DNA damage
rottlerin
PKC-δ
PKC
HeLA cells
Cell and Developmental Biology
Cell Biology
Cells
Cellular and Molecular Physiology
Life Sciences
Medical Cell Biology
Medical Genetics
Medicine and Health Sciences
Other Cell and Developmental Biology
Basal P53
protein kinase C
anticancer-drug induced apoptosis
tumor suppression protein
DNA damage
rottlerin
PKC-δ
PKC
HeLA cells
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