Embryonal stem cells do not undergo cell cycle arrest upon exposure to damaging factors

As shown recently (Malashicheva et al., 2000), embryonic teratocarcinoma F9 mouse cells do not stop on the G1/S border after the treatment with agents causing G1 arrest in normal fibroblast cells. Since after a prolonged cultivation in vitro F9 cells could lose some properties characteristic of the...

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Bibliographic Details
Published in:	T͡S︡itologii͡a Vol. 44; no. 7; p. 643
Main Authors:	Malashicheva, A B, Kisliakova, T V, Savatier, P, Pospelov, V A
Format:	Journal Article
Language:	Russian
Published:	Russia (Federation) 2002
Subjects:	Acetylcysteine - analogs & derivatives Acetylcysteine - pharmacology Animals Aspartic Acid - analogs & derivatives Aspartic Acid - pharmacology Cell Cycle - drug effects Cell Cycle - radiation effects Cell Line Cyclin-Dependent Kinase Inhibitor p21 Cyclins - metabolism Doxorubicin - pharmacology Embryo, Mammalian - cytology Embryo, Mammalian - metabolism Mice Nocodazole - pharmacology Phosphonoacetic Acid - analogs & derivatives Phosphonoacetic Acid - pharmacology Stem Cells - cytology Stem Cells - metabolism Tumor Cells, Cultured
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Summary:	As shown recently (Malashicheva et al., 2000), embryonic teratocarcinoma F9 mouse cells do not stop on the G1/S border after the treatment with agents causing G1 arrest in normal fibroblast cells. Since after a prolonged cultivation in vitro F9 cells could lose some properties characteristic of the stem cells, we studied here the capability of mouse ES cells to undergo cell cycle blocks following gamma-irradiation, adriamycin and PALA treatment as well as upon cultivation in the presence of nocodazol, an inhibitor of spindle assembly. The results obtained show that ES cells, similarly as their tumorigenic derivative F9 cells, do not demonstrate any delay on the G1/S boundary of the cell cycle. Moreover, nocodazol treatment for 48 h leads to accumulation of polyploid cells. Immunoblot experiments reveal a low level of p21/Waf1 expression both in F9 and in ES cells. Interestingly, the content of p21/Waf1 has been found to increase after cell treatment with proteasome inhibitor lactacystin, implying that p21/Waf1 level is regulated by proteasomal degradation. Thus, the p21/Waf1--dependent mechanisms of cell cycle control (checkpoint control) do not function properly in embryonic stem cells.
ISSN:	0041-3771