摘要
鼠双微体2（MDM2）基因是电离和紫外线辐射反应中的关键组分,MDM2表达水平决定辐射诱导的抑癌基因p53活性增加程度。MDM2可以限制p53的凋亡功能,是许多类型细胞的存活因子。另外,DNA损伤诱导MDM2的表达,一般认为高水平的MDM2蛋白可以缩短辐射后p53建立的细胞周期阻滞。MDM2表达的增加似乎可以保证存活细胞中p53的活性回复到较低的基础水平。MDM2水平的降低增加了细胞对电离辐射的敏感性。因此,MDM2是介入治疗的潜在靶点。
Murine double minute 2 （MDM2） gene is a eritieal eomponent of the responses to both ionizing and UV radiation. The level of MDM2 expression determines the extent to whieh radiation induees an inerease in the aetivity of the p53 tumor suppressor. MDM2 aets as a survival faetor in many eell types by limiting the apoptotie funetion of p53. In addition, expression of MDM2 is indueed in response to DNA damage, and the resulting high levels of MDM2 protein are thought to shorten the length of the eell eyele arrest established by p53 in the radiation response. Inereased levels of MDM2 appear to ensure that the aetivity of p53 returns to its low basal levels in surviving eells. Deereased levels of MDM2 sensitize eells to radiation. Thus, MDM2 is a potential target for therapeutie intervention beeause its inhibition may radiosensitize the subset of human tumors expressing wild-type p53 sueh that radiotherapy is more efficaeious.
出处
《国际放射医学核医学杂志》
2007年第2期118-121,共4页
International Journal of Radiation Medicine and Nuclear Medicine
