INVOLVEMENT OF MAP-KINASE CASCADES INTO THE REGULATION OF SODIUM BYTURATE INDUCED PREMATURE CELL SENESCENCE
E.Yu. Kochetkova, T.V. Bykova, S.G. Zubova, T.V. Pospelova
Institute of Cytology RAS, Saint-Petersburg State University, Saint-Petersburg;
e-mail: lena.linnaea@gmail.com
We studied the role of p38 kinase and JNK1, 2 in the activation of the complex mTORC1 and senescence program induced by histone deacetylase inhibitor sodium butyrate
(NaBut) in mouse embryonic fibroblasts transformed by E1A+cHa-Ras oncogenes. It was found that transformants from knockouts for the genes p38, are able to
implement a program of NaBut- induced senescence, according to the data of the cell cycle arrest, inhibition of proliferation, hypertrophic changes associated with the activation
of mTORC1 and SA-β-galactosidase activity. According to behavior of these markers, cell knockouts for the genes jnk1,2, were unable to implement NaBut-induced
senescence. Induction of senescence closely correlates with the activation of the complex mTORC1, as it was shown by inhibiting mTORC1 with rapamycin. We believe that
JNK 1,2 kinases are required for mTORC1 activation and acquiring the markers of premature senescence, induced by NaBut in the E1A+cHa-Ras transformants.
Key words: TOR, mTORC1, JNK, p38, sodium byturate, premature cell senescence
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