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Increased Rac activity is required for the progression of T-lymphomas induced by Pten-deficiency.

Abstract：

:Mutation of the tumor suppressor PTEN results in loss of its PI3-kinase counteracting function. PI3-kinase stimulates tumor formation by PKB/Akt-mediated cell proliferation and prevention of apoptosis. PI3-kinase may also activate Rho-GTPases and their regulatory GEFs to promote invasion. Here we have analyzed the function of the Rac-specific activator, Tiam1, in PI3-kinase-induced T-lymphomagenesis. Mice with a T cell-specific Pten deletion developed T-lymphomas with enhanced PKB/Akt phosphorylation. However, these T-lymphomas infiltrated more frequently into various organs in Tiam1-deficient mice compared to wild type mice. Surprisingly, Tiam1-deficient lymphomas showed increased Rac activity, suggesting that the lack of Tiam1 is compensated by alternative Rac-activating mechanisms that lead to increased progression of PI3-kinase-induced T-lymphomas.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Strumane K,Song JY,Baas I,Collard JG

doi

10.1016/j.leukres.2007.03.034

subject

Has Abstract

pub_date

2008-01-01 00:00:00

pages

113-20

issue

1

eissn

0145-2126

issn

1873-5835

pii

S0145-2126(07)00127-0

journal_volume

32

pub_type

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