Cellular quiescence caused by the Mdm2 inhibitor nutlin-3a

被引：54

作者：

Korotchkina, Lioubov G. ^{[1
]}

Demidenko, Zoya N. ^{[2
]}

Gudkov, Andrei V. ^{[1
]}

Blagosklonny, Mikhail V. ^{[1
]}

机构：

[1] BLSC, Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY USA

[2] Oncotarget, Buffalo, NY USA

来源：

CELL CYCLE | 2009年 / 8卷 / 22期

关键词：

senescence; p53; p21; quiescence; cell cycle; SMALL-MOLECULE ANTAGONISTS; P53-MDM2; BINDING; GROWTH ARREST; TUMOR-CELLS; P53; PATHWAY; IN-VIVO; SENESCENCE; ACTIVATION; SENSITIVITY; APOPTOSIS;

D O I：

10.4161/cc.8.22.10121

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cellular senescence is characterized by irreversible loss of proliferative potential and a large, flat cell morphology. Ectopic p21 and doxorubicin induced cellular senescence in HT1080 and WI-38-tert cell lines. In the same cell lines, the Mdm2 inhibitor nutlin-3a induced p53 but, unexpectedly, caused quiescence (reversible arrest) with a small cell morphology. We discuss that Mdm antagonists could be used in combination with chemotherapy to reversibly arrest normal cells, thus protecting them during chemotherapy of cancer (cyclotherapy).

引用

页码：3777 / 3781

页数：5

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