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Erbin loss promotes cancer cell proliferation through feedback activation of Akt-Skp2-p27 signaling.

Abstract：

:Erbin localizes at the basolateral membrane to regulate cell junctions and polarity in epithelial cells. Dysregulation of Erbin has been implicated in tumorigenesis, and yet it is still unclear if and how disrupted Erbin regulates the biological behavior of cancer cells. We report here that depletion of Erbin leads to cancer cell excessive proliferation in vitro and in vivo. Erbin deficiency accelerates S-phase entry by down-regulating CDK inhibitors p21 and p27 via two independent mechanisms. Mechanistically, Erbin loss promotes p27 degradation by enhancing E3 ligase Skp2 activity though augmenting Akt signaling. Interestingly, we also show that Erbin is an unstable protein when the Akt-Skp2 signaling is aberrantly activated, which can be specifically destructed by SCF-Skp2 ligase. Erbin loss facilitates cell proliferation and migration in Skp2-dependent manner. Thus, our finding illustrates a novel negative feedback loop between Erbin and Akt-Skp2 signaling. It suggests disrupted Erbin links polarity loss, hyperproliferation and tumorigenesis.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Huang H,Song Y,Wu Y,Guo N,Ma Y,Qian L

doi

10.1016/j.bbrc.2015.05.071

subject

Has Abstract

pub_date

2015-07-31 00:00:00

pages

370-6

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)00994-8

journal_volume

463

pub_type

杂志文章

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