Trigiante Giuseppe, Lu Xin
Ludwig Institute for Cancer Research, Courtauld Building, 91 Riding House Street, London W1W 7BS, UK.
Nat Rev Cancer. 2006 Mar;6(3):217-26. doi: 10.1038/nrc1818.
One of the most frequently mutated genes in human cancers, tumour suppressor p53 (TP53), can induce cell-cycle arrest and apoptosis. The apoptotic function of p53 is tightly linked to its tumour-suppression function and the efficacy of many cancer therapies depends on this. The identification of a new family of proteins, known as ASPPs (ankyrin-repeat-, SH3-domain- and proline-rich-region-containing proteins), has led to the discovery of a novel mechanism that selectively regulates the apoptotic function, but not the cell-cycle-arrest function, of p53, and gives an insight into how p53 responds to different stress signals. ASPPs might be new molecular targets for cancer therapy.
肿瘤抑制因子p53(TP53)是人类癌症中最常发生突变的基因之一,它可诱导细胞周期停滞和凋亡。p53的凋亡功能与其肿瘤抑制功能紧密相关,许多癌症治疗的疗效也取决于此。一种被称为ASPPs(含锚蛋白重复序列、SH3结构域和富含脯氨酸区域的蛋白质)的新蛋白质家族的发现,促成了一种新机制的发现,该机制可选择性地调节p53的凋亡功能,而非其细胞周期停滞功能,并深入揭示了p53如何应对不同的应激信号。ASPPs可能是癌症治疗的新分子靶点。