Zhang Chris Z Y, Chen George G, Lai Paul B S
Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong.
Biochim Biophys Acta. 2010 Aug;1806(1):36-41. doi: 10.1016/j.bbcan.2010.03.002. Epub 2010 Mar 15.
ZBP-89, a Krüppel-type zinc-finger transcription factor that binds to GC-rich sequences, is involved in the regulation of cell growth and cell death. It maps to chromosome 3q21 and is composed of 794 residues. Having bifunctional regulatory domains, ZBP-89 may function as a transcriptional activator or repressor of variety of genes such as p16 and vimentin. ZBP-89 arrests cell proliferation through its interactions with p53 and p21(waf1). It is able to stabilize p53 through directly binding and enhance p53 transcriptional activity by retaining it in the nucleus. In addition, ZBP-89 potentiates in butyrate-induced endogenous p21(waf1) up-regulation. ZBP-89 is usually over-expressed in human cancer cells, where it can efficiently induce apoptosis through p53-dependent and -independent mechanisms. Moreover, ZBP-89 is capable of enhancing killing effects of several anti-cancer drugs. Therefore, ZBP-89 may be served as a potential target in cancer therapy.
ZBP-89是一种与富含GC序列结合的Krüppel型锌指转录因子，参与细胞生长和细胞死亡的调控。它定位于3号染色体q21区域，由794个氨基酸残基组成。ZBP-89具有双功能调节结构域，可能作为多种基因（如p16和波形蛋白）的转录激活剂或抑制剂发挥作用。ZBP-89通过与p53和p21（waf1）相互作用来阻止细胞增殖。它能够通过直接结合来稳定p53，并通过将其保留在细胞核中来增强p53的转录活性。此外，ZBP-89增强丁酸盐诱导的内源性p21（waf1）上调。ZBP-89通常在人类癌细胞中过度表达，在那里它可以通过p53依赖和非依赖机制有效诱导凋亡。此外，ZBP-89能够增强几种抗癌药物的杀伤作用。因此，ZBP-89可能成为癌症治疗的潜在靶点。
