摘要
p53基因家族新成员p73与其同源体p53在结构和功能上都具有高度相似性。p73基因过表达能够激活p53的靶基因从而诱导细胞凋亡,也能对异常的细胞增殖和一些DNA损伤事件产生反应性活化,同时因为p73在1p36的特殊定位,研究者认为p73基因或许像p53一样是一个肿瘤抑制基因。但是,p73基因敲除鼠并不发生自发性肿瘤,肿瘤中极少发现p73基因的突变,N末端转录活化区丢失的异构体ΔNp73具有与全长p73基因相反的功能,ΔTA p73更象一个癌基因起着促进肿瘤生长的作用。就p73及其异构体ΔTA p73在人类肿瘤中的矛盾表现及近期研究进展予以综述。
p73 is a new member of the p53 family of proteins. As p53, its homologue p73 has significant sequence and functional similarties. Overexpression of p73 can activate typical p53 responsive genes, and activation of p73 is implicated in apoptotic cell death induced by aberrant cell proliferation and some form of DNA-damage. These data together with the localization of p73 on chromosome 1p36, a special region, led to the hypothesis that p73 has tumor suppressor activity just like p53. However, p73 knockout mice do not develop tumors. Few mutations of p73 have been found in spit of extensive studies in tumors. ΔTA-p73, an isoform of p73 that lacks the transactivation domain, seems to function as an oncogene. In the light of these new findings the contradictory role of p73 and ΔTA-p73 in malignancy is discussed. This review summarizes some aspects of this “two in one” gene’s biology with particular reference to its possible role in cancer.
出处
《肿瘤防治杂志》
2005年第7期551-554,共4页
China Journal of Cancer Prevention and Treatment
