Cellular quiescence caused by the Mdm2 inhibitor nutlin-3a
Cellular quiescence caused by the Mdm2 inhibitor nutlin-3a
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DOI：
10.4161/cc.8.22.10121
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发表时间：
2009-11-15
期刊：
影响因子：
4.3
通讯作者：
Blagosklonny, Mikhail V.
中科院分区：
文献类型：
--
作者：
Korotchkina, Lioubov G.;Demidenko, Zoya N.;Blagosklonny, Mikhail V.
细胞衰老的特征在于不可逆的增殖潜能丧失和大而扁平的细胞形态。异位p21和阿霉素诱导HT 1080和WI-38-tert细胞系的细胞衰老。在相同的细胞系中，Mdm 2抑制剂nutlin-3a诱导p53，但出乎意料地，引起静止（可逆停滞）与小细胞形态。我们讨论了Mdm拮抗剂可以与化疗联合使用，以可逆地阻止正常细胞，从而在癌症化疗（化疗）期间保护它们。
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).