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IkappaB kinase promotes tumorigenesis through inhibition of forkhead FOXO3a.

Abstract：

:Nuclear exclusion of the forkhead transcription factor FOXO3a by protein kinase Akt contributes to cell survival. We investigated the pathological relationship between phosphoylated-Akt (Akt-p) and FOXO3a in primary tumors. Surprisingly, FOXO3a was found to be excluded from the nuclei of some tumors lacking Akt-p, suggesting an Akt-independent mechanism of regulating FOXO3a localization. We provide evidence for such a mechanism by showing that IkappaB kinase (IKK) physically interacts with, phosphorylates, and inhibits FOXO3a independent of Akt and causes proteolysis of FOXO3a via the Ub-dependent proteasome pathway. Cytoplasmic FOXO3a correlates with expression of IKKbeta or Akt-p in many tumors and associates with poor survival in breast cancer. Further, constitutive expression of IKKbeta promotes cell proliferation and tumorigenesis that can be overridden by FOXO3a. These results suggest the negative regulation of FOXO factors by IKK as a key mechanism for promoting cell growth and tumorigenesis.

journal_name

Cell

journal_title

Cell

authors

Hu MC,Lee DF,Xia W,Golfman LS,Ou-Yang F,Yang JY,Zou Y,Bao S,Hanada N,Saso H,Kobayashi R,Hung MC

doi

10.1016/s0092-8674(04)00302-2

subject

Has Abstract

pub_date

2004-04-16 00:00:00

pages

225-37

issue

2

eissn

0092-8674

issn

1097-4172

pii

S0092867404003022

journal_volume

117

pub_type

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