CD95-mediated apoptosis: no variation in cellular sensitivity during cell cycle progression.
Sensitivity of CD95-mediated apoptosis has been reported to vary during cell cycle progression (FEBS Lett. (1997) 412, 91-93). Here, we report that three human glioma cell lines with different p53 status (i) undergo growth arrest and synchronous cell cycle re-entry after prolonged serum deprivation, (ii) do not exhibit cell cycle-related changes in CD95 expression at the cell surface, and (iii) do not exhibit cell cycle-related changes in susceptibility to DC95 ligand-induced apoptosis. In contrast, cell cycle-specific activity was demonstrated for various cancer chemotherapy drugs. Further, CD95 expression and susceptibility to CD95 ligand-induced apoptosis does not vary during cell cycle progression of Jurkat T cells, HeLa cervical carcinoma and HepG2 hepatocellular carcinoma cells. These results do not support a role for the cell cycle phase as an important predictor of vulnerability to CD95-mediated apoptosis.
Hueber
A
A
Department of Neurology, University of Tübingen, School of Medicine, Germany.
Durka
S
S
Weller
M
M
D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology; D000972:Antineoplastic Agents, Phytogenic; D016590:Aphidicolin / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology* / Q000502:physiology; D002166:Camptothecin / Q000494:pharmacology; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology; D016923:Cell Death / Q000187:drug effects; D002945:Cisplatin / Q000494:pharmacology; D016895:Culture Media, Serum-Free / Q000494:pharmacology; D004317:Doxorubicin / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D053222:Fas Ligand Protein; D015870:Gene Expression / Q000235:genetics; D006367:HeLa Cells; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D019169:Jurkat Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000494:pharmacology; D015376:Nimustine / Q000494:pharmacology; D015739:Nocodazole / Q000494:pharmacology; D017239:Paclitaxel / Q000494:pharmacology; D012680:Sensitivity and Specificity; D013713:Teniposide / Q000494:pharmacology; D014407:Tumor Cells, Cultured / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D014750:Vincristine / Q000494:pharmacology; D019014:fas Receptor / Q000187:drug effects / Q000235:genetics / Q000502:physiology*
D000903:Antibiotics, Antineoplastic; D000970:Antineoplastic Agents; D000972:Antineoplastic Agents, Phytogenic; D016895:Culture Media, Serum-Free; D004791:Enzyme Inhibitors; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor; D015376:Nimustine; D016590:Aphidicolin; D014750:Vincristine; D004317:Doxorubicin; D013713:Teniposide; D017239:Paclitaxel; D002945:Cisplatin; D015739:Nocodazole; D006918:Hydroxyurea; D002166:Camptothecin