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p57Kip2属于细胞周期依赖激酶抑制因子(cyclin dependent kinases inhibitor,CDKI)Cip/Kip家族的成员之一,CKI能竞争性地与细胞周期蛋白依赖性激酶(cyclin dependent kinase,CDK)结合抑制其活性,从而调整细胞周期。与家族其它成员相比,p57Kip2在结构和功能有其特殊性。p57Kip2通过多种机制参与肿瘤的发生、侵袭和转移过程,Cip/Kip蛋白能在不同水平抑制Rho/ROCK/LIM/coffilin信号通路而参与肿瘤的形成、侵袭和转移,但在不同的细胞定位和调控下,p57Kip2在肿瘤的侵袭和转移中扮演双重角色。p57Kip2在细胞分化、凋亡上也具有重要作用,p57Kip2的表达异常使细胞不分化和过度增殖而形成肿瘤,p57Kip2在细胞凋亡中的作用也许可以作为肿瘤治疗的靶点。多功能的p57Kip2通过印记丢失、杂合性缺失、启动子甲基化、组蛋白去乙酰化和microRNA的调控等参与肿瘤形成的多个过程。本文就p57Kip2在以上几个方面的研究进展做一综述。
p57Kip2 is a member of the Cip / Kip family of cyclin dependent kinase inhibitors (CDKIs), and CKI competitively binds to cyclin dependent kinase (CDK) to inhibit its activity Adjust cell cycle. Compared with other members of the family, p57Kip2 has its own structure and function. P57Kip2 participates in the process of tumorigenesis, invasion and metastasis through a variety of mechanisms. Cip / Kip protein can inhibit the formation, invasion and metastasis of Rho / ROCK / LIM / coffilin signaling pathway at different levels. However, Regulation, p57Kip2 plays a dual role in tumor invasion and metastasis. p57Kip2 also plays an important role in cell differentiation and apoptosis. The abnormal expression of p57Kip2 makes the cells undifferentiated and over-proliferated to form tumors. The role of p57Kip2 in apoptosis may be used as a target for tumor therapy. Multifunctional p57Kip2 is involved in multiple processes of tumor formation through loss of imprinting, loss of heterozygosity, promoter methylation, histone deacetylation and regulation of microRNAs. This article reviews the progress of p57Kip2 in the above aspects.