p57是细胞周期蛋白依赖性激酶（CDK）抑制剂，这是第一个受印迹调控的细胞周期调节剂。基于p57通过其N端结构域调节细胞周期进程的能力，最初被认为是一种肿瘤抑制因子。现在，已经发现p57还通过其PAPA重复序列和羧基末端结构域参与其他细胞过程的调节，包括转录，凋亡，分化，发育和迁移。p57的多功能参与肿瘤发生的许多过程，涉及不同的机制，包括印迹的丧失，杂合性的丧失，启动子甲基化，组蛋白脱乙酰化和microRNA的调控。此外，上游信号通路 蛋白-蛋白相互作用和亚细胞定位的改变也据报道参与p57的异常表达，导致癌症的发生和发展。然而，尚不清楚p57是否与其同胞在不同细胞过程下的肿瘤发生过程中起双重作用。p57中存在核定位信号很有趣，因为它可能影响p57的亚细胞定位，这可能导致细胞异常增殖和运动，并且在某些情况下可能致癌，如p21和p27所观察到的。
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p57: A multifunctional protein in cancer (Review).
p57 is a cyclin-dependent kinase (CDK) inhibitor, the first cell cycle regulator that is regulated by imprinting. p57 was initially considered to be a tumor suppressor based on its ability to regulate cell cycle progression through its N-terminal domain. Now, it has been found that p57 is also involved in the regulation of other cellular processes including transcription, apoptosis, differentiation, development, and migration via its PAPA repeat and carboxyl-terminal domain. The multifunction of p57 participate in many processes in tumorigenesis involving in different mechanisms including loss of imprinting, loss of heterozygosity, promoter methylation, histone deacetylation and regulation of microRNAs. Moreover, upstream signaling pathways, protein-protein interactions and altered subcellular localization have also been reported to participate in abnormal expression of p57 resulting in the occurrence and progression of cancer. However, it is unclear whether p57 may play a dual role during tumorigenesis under different cellular processes similarly to its siblings. The presence of a nuclear localization signal in p57 is intriguing because it may affect the subcellular localization of p57, which can result in abnormal proliferation and motility of cells, and may be oncogenic under certain circumstances, as observed for p21 and p27.
