Electroporation and carrier DNA cause p53 activation, cell cycle arrest, and apoptosis.
Methods used in transient transfection of cells may alter cellular signaling pathways that in turn may lead to misinterpretation of the results. A variety of genotoxic agents cause the accumulation of the p53 protein leading to either apoptosis or growth arrest. Here we report the effect of electroporation and carrier DNA on the stability, cellular localization, and transcriptional activity of p53. We show that electroporation leads to p53-dependent and also p53-independent cell-cycle arrest and apoptosis. At the same time a chemical agent polyethylenimine that is also used for transient transfection of cells causes neither upregulation of p53 nor cellular response.
Lepik
Dina
D
Department of Cell Biology, Institute of Molecular and Cell Biology, Tartu University, 23 Riia Street, Tartu 51010, Estonia. dlepik@ebc.ee
Jaks
Viljar
V
Kadaja
Lilian
L
Värv
Signe
S
Maimets
Toivo
T
D000818:Animals; D017209:Apoptosis; D002417:Cattle; D002453:Cell Cycle; D045744:Cell Line, Tumor; D004278:DNA, Superhelical / Q000378:metabolism* / Q000494:pharmacology; D018274:Electroporation; D006801:Humans; D051379:Mice; D041681:NIH 3T3 Cells; D011094:Polyethyleneimine / Q000494:pharmacology; D014162:Transfection / Q000379:methods; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000378:metabolism*
D004278:DNA, Superhelical; D016159:Tumor Suppressor Protein p53; D011094:Polyethyleneimine