Vousden Karen H
Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.
J Cell Sci. 2006 Dec 15;119(Pt 24):5015-20. doi: 10.1242/jcs.03293.
The p53 tumour suppressor protein can efficiently inhibit tumour development. This activity reflects its ability to induce a number of different responses, including cell cycle arrest and apoptosis. Recent studies have revealed some interesting insights into how the choice of response to p53 is regulated, highlighting a correlation between the activation of cell cycle arrest and survival with the ability of p53 to reduce oxidative stress and protect cells from genotoxic damage. Understanding the molecular mechanisms that determine which response is selected may allow us to modulate these pathways so that therapeutic reactivation of p53 favours apoptotic cell death in tumour cells, but a reversible--and therefore far less toxic--induction of cell cycle arrest in normal cells.
p53肿瘤抑制蛋白能够有效抑制肿瘤发展。这种活性反映了它诱导多种不同反应的能力，包括细胞周期停滞和细胞凋亡。最近的研究揭示了一些关于p53反应选择如何被调控的有趣见解，突出了细胞周期停滞和存活的激活与p53降低氧化应激及保护细胞免受基因毒性损伤能力之间的相关性。了解决定选择哪种反应的分子机制可能使我们能够调节这些途径，从而使p53的治疗性重新激活有利于肿瘤细胞的凋亡性细胞死亡，但在正常细胞中诱导细胞周期停滞是可逆的——因此毒性要小得多。
