ASPP2 is a haploinsufficient tumor suppressor that cooperates with p53 to suppress tumor growth

被引：87
|
作者：
Vives, Virginie
Su, Jian
Zhong, Shan
Ratnayaka, Indrika
Slee, Elizabeth
Goldin, Robert
Lu, Xin
机构：
[1] UCL, Ludwig Inst Canc Res, London W1W 7BS, England
[2] Univ London Imperial Coll Sci Technol & Med, Fac Med, St Marys, Dept Pathol, London W2 1PG, England
来源：
GENES & DEVELOPMENT | 2006年 / 20卷 / 10期
关键词：
D O I：
10.1101/gad.374006
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
ASPP2 stimulates the apoptotic function of the p53 family in vivo. We show here that ASPP2(-/-) pups died before weaning. This postnatal lethality was significantly enhanced in p53(+/-) background and both deletions are synthetic lethal. ASPP2(+/-) mice developed spontaneous tumors. The tumor onset was accelerated by gamma-irradiation or in p53(+/-) background. Tumors derived from ASPP2(+/-)mice retained wild-type ASPP2 allele even though some of them lost p53. These provide the first genetic evidence that ASPP2 is a haploinsufficient tumor suppressor that shares overlapping function(s) with p53 in mouse development and tumor suppression.
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收藏
页码：1262 / 1267
页数：6
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