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首页> 外文期刊>Cancer Cell >Is Cyclin D1-CDK4 kinase a bona fide cancer target?
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Is Cyclin D1-CDK4 kinase a bona fide cancer target?

机译:Cyclin D1-CDK4激酶是否是真正的癌症靶标?

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摘要

Previous studies have demonstrated that mice lacking Cyclin D1 were refractory to mammary tumor development induced by the c-neu/erbB-2 oncogene, the rodent ortholog of the HER-2 receptor frequently overexpressed in human breast carcinomas. Two new studies in this issue of Cancer Cell provide additional evidence on this issue. Knockin mice expressing a mutant form of Cyclin D1 that binds to Cdk4/6 but cannot activate their catalytic activity are resistant to c-neu/erbB-2 tumorigenesis in spite of undergoing normal epithelial cell expansion during pregnancy. Moreover, knockdown of Cdk4 in mammary tumor cells abrogates tumor formation. These observations provide new compelling evidence that inhibition of Cyclin D1-Cdk4/6 kinases might be beneficial for cancer therapy.
机译:先前的研究表明,缺乏Cyclin D1的小鼠对c-neu / erbB-2致癌基因(HER-2受体的啮齿动物直系同源物在人类乳腺癌中经常过度表达)诱导的乳腺肿瘤发展具有难治性。本期《癌细胞》的两项新研究提供了有关此问题的其他证据。尽管在怀孕期间经历了正常的上皮细胞扩增,但表达与Cdk4 / 6结合但不能激活其催化活性的Cyclin D1突变形式的敲敲小鼠对c-neu / erbB-2肿瘤发生具有抵抗力。此外,在乳腺肿瘤细胞中敲除Cdk4可消除肿瘤形成。这些发现提供了令人信服的新证据,即抑制Cyclin D1-Cdk4 / 6激酶可能对癌症治疗有益。

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