CK2 functionally interacts with AKT/PKB to promote the ß-catenin-dependent expression of survivin and enhance cell survival.
Mol Cell Biochem
; 356(1-2): 127-32, 2011 Oct.
Article
em En
| MEDLINE
| ID: mdl-21735093
ABSTRACT
ß-Catenin is crucial in the canonical Wnt signaling pathway. This pathway is up-regulated by CK2 which is associated with an enhanced expression of the antiapoptotic protein survivin, although the underlying molecular mechanism is unknown. AKT/PKB kinase phosphorylates and promotes ß-catenin transcriptional activity, whereas CK2 hyperactivates AKT by phosphorylation at Ser129; however, the role of this phosphorylation on ß-catenin transcriptional activity and cell survival is unclear. We studied in HEK-293T cells, the effect of CK2-dependent hyperactivation of AKT on cell viability, as well as analyzed ß-catenin subcellular localization and transcriptional activity and survivin expression. CK2α overexpression led to an augmented ß-catenin-dependent transcription and protein levels of survivin, and consequently an enhanced resistance to apoptosis. However, CK2α-enhancing effects were reversed when an AKT mutant deficient in Ser129 phosphorylation by CK2 was co-expressed. Therefore, our results strongly suggest that CK2α-specific enhancement of ß-catenin transcriptional activity as well as cell survival may depend on AKT hyperactivation by CK2.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Caseína Quinase II
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Proteínas Proto-Oncogênicas c-akt
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Proteínas Inibidoras de Apoptose
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Beta Catenina
Limite:
Humans
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article