CDKs与癌症关系的研究进展

Investigative progress of relation of CDKs and cancer

CDKs活性的改变将介导肿瘤相关的细胞周期缺陷。失去调控的CDKs诱导无限制的增殖和基因及染色体的不稳定性。根据通常的模式,哺乳动物CDKs对细胞周期的进程很关键,以至于阻碍CDK活性的化疗不能选择性的靶定肿瘤细胞。遗传学资料表明CDK1对细胞周期是必需的,而且分裂间期CDKs对特殊细胞的增殖是非常重要的。最新研究表明肿瘤细胞的增殖也需要特殊的分裂间期CDKs。因此,选择性的抑制CDK有利于人类某种肿瘤的治疗。

Tumour-associated cell cycle defects are often mediated by alterations of incyclin-dependent kinase （CDK） activity. Misregulated CDKs induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models,mammalian CDKs are essential for driving each cell cycle phase, so therapeutic strate- gies that block CDK activity are unlikely to selectively target tumour cells. However, recent genetic evidence has revealed that, whereas CDK1 is required for the cell cycle, interphase CDKs are only essential for proliferation of spe- cialized cells. Emerging evidence suggests that tumour cells may also require specific interphase CDKs for proliferation. Thus, selective CDK inhibition may provide therapeutic benefit against certain human neoplasias.