SODIUM BUTYRATE DO NOT INDUCE THE PROGRAM OF PREMATURE SENESCENCE IN TRANSFORMANTS WITH JNK1,2 KNOCKOUT
S. G. Zubova, T. V. Bykova, J. G. Zubova, V. S. Romanov, N. D. Aksenov, V. A. Pospelov, T. V. Pospelova
Institute of Cytology RAS, St. Petersburg;
e-mail: egretta_jlia@mail.ru
We studied the role of JNK1,2 stress-kinases in the regulation of premature senescence program, stimulated by the inhibitor of histone deacetylase, sodium
butyrate (NaB). It was found, that the transformants E1A + cHa-ras selected from embryonic mouse fibroblasts with knockout jnk1,2 stress-kinase
genes did not block the cell cycle after sodium butyrate treatment. The data on the cell cycle distribution and cell growth curves showed that even long term (during
five days) NaB influence did not suppress proliferation. We did not also reveal any cellular hypertrophy and increase in SA-β-galactosidase activity after NaB
treatment. The data presented suggest that JNK stress-kinases are involved in sodium butyrate-induced senescence in E1A + cHa-ras mouse transformants,
and they are indicative of that JNK1,2 have tumor suppressor properties.
Key words: oncogenes E1A and cHa-ras, transformation, JNK1,2 kinase, senescence, cell cycle, sodium butyrate
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