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Bcl-xL gain of function and p19 ARF loss of function cooperate oncogenically with Myc in vivo by distinct mechanisms.

Abstract：

:Overexpression of Bcl-xL, loss of p19 ARF, and loss of p53 all accelerate Myc oncogenesis. All three lesions are implicated in suppressing Myc-induced apoptosis, suggesting that this is a common mechanism by which they synergize with Myc. However, using an acutely switchable model of Myc-induced tumorigenesis, we demonstrate that each lesion cooperates with Myc in vivo by a distinct mechanism. While Bcl-xL blocks Myc-induced apoptosis, inactivation of p19 ARF enhances it. However, this increase in apoptosis is matched by increased Myc-induced proliferation. p53 inactivation shares features of both lesions, partially suppressing apoptosis while augmenting proliferation. Bcl-xL and p19 ARF loss together synergize to further accelerate Myc oncogenesis. Thus, differing lesions cooperate oncogenically with Myc by discrete mechanisms that can themselves synergize with each other.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Finch A,Prescott J,Shchors K,Hunt A,Soucek L,Dansen TB,Swigart LB,Evan GI

doi

10.1016/j.ccr.2006.06.017

subject

Has Abstract

pub_date

2006-08-01 00:00:00

pages

113-20

issue

2

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(06)00215-7

journal_volume

10

pub_type

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