Apoptosis and perturbation of cell cycle progression in an acidic environment after hyperthermia.
The effects of an acidic environment on the induction of apoptosis by 42 degrees C hyperthermia were investigated. An acidic environment (pH 6.6) enhanced the hyperthermia-induced apoptosis in HL-60 human promyelocytic leukemia cells as judged by the DNA fragmentation, flow cytometric analysis of DNA content, and cleavage of poly(ADP-ribose) polymerase. Hyperthermia exerted no effect on the expression of Bcl-2 and Bax, regardless of the environmental acidity during heating. The time of increase in apoptosis after heating coincided with the time of decrease in the G1-phase cell population. It seemed that the increase in heat-induced apoptosis in HL-60 cells in an acidic environment was due to a direct increase in the proteolytic cleavage of poly(ADP-ribose) polymerase by acidic caspases without the involvement of Bcl-2 and Bax, and that heat-induced apoptosis occurred during G1 phase in HL-60 cells.
Takasu
T
T
Department of Therapeutic Radiology-Radiation Oncology, University of Minnesota Medical School, Minneapolis 55455, USA.
Lyons
J C
JC
Park
H J
HJ
Song
C W
CW
D017209:Apoptosis / Q000235:genetics; D002453:Cell Cycle; D053938:DNA Fragmentation; D004273:DNA, Neoplasm; D004587:Electrophoresis, Agar Gel; D005434:Flow Cytometry; D019254:Genes, bcl-2 / Q000502:physiology; D018922:HL-60 Cells; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006979:Hyperthermia, Induced; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein
C494826:BAX protein, human; D004273:DNA, Neoplasm; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D011065:Poly(ADP-ribose) Polymerases