中文摘要：

人程序性细胞死亡因子10（programmed cell death 10,PDCD10）最初被称为TFAR15（TF-1 cell apoptosis related gene 15）,是在1999年运用cDNA-RDA技术首先克隆得到的一个新基因,早期研究提示与凋亡抑制功能相关.近期国外多项研究证明,PDCD10基因的缺失和突变与颅内海绵状血管瘤（cerebral cavernous malformations,CCM）的发生密切相关,CCM的第三个致病基因CCM3即为PDCD10.此外,其他研究表明,PDCD10受到严格的表达调控,在多种肿瘤组织中表达明显上调,提示可能在肿瘤的信号转导通路中起重要作用.最近通过对PDCD10相互作用蛋白的分析和研究,首次证实了PDCD10可以和Ste20激酶家族成员MST4相互作用,增强其激酶活性,并进而通过对ERK-MAPK通路的调控,促进细胞增殖和转化.以上研究证明了PDCD10的多种生物学效应,并提示其在血管生成和肿瘤中发挥重要作用.

英文摘要：

Homo sapiens PDCDIO （programmed cell death 10, alias, ＂TF-1 cell apoptosis related gene 15, TFAR15＂ ）, cloned by means of cDNA-representational differences analysis, had been initially identified associated with cell apoptosis. Recent research suggested mutations within the PDCDIO gene or deletion were responsible for cerebral cavernous malformations, and PDCDIO was the third CCM gene. On the other hand, other research demonstrated that PDCD 10 was strictly modulated and up regulated in many kinds of tumors, which implicated that PDCD 10 participated in tumorous signal transduction. The recent research confirmed that PDCD 10 interacts with MST4, a member of Ste20-related kinases, and the interaction promoted cell proliferation and transformation via modulation of the ERK-MARK pathway. In conclusion, all these demonstrate that PDCD10 has many biological effects, which suggests that it is a novel player in vascular morphogenesis and/or remodeling, as well as tumorigenesis and cancer progression.