HHV-8感染与PI3K/Akt/mTOR信号转导通路研究进展  

The Study Progress about Human Herpesivirus-8 Infection and Phosphatidylinositol 3-kinase-Akt Signal Transduction Pathway

作　　者：张慧[1] 杨磊[1] 

机构地区：[1]石河子大学新疆地方病与民族高发病省部共建教育部重点实验室

出　　处：《医学综述》2009年第10期1441-1444,共4页Medical Recapitulate

基　　金：国际科技合作项目(2005DFA30780);教育部科学研究重大项目(206166)

摘　　要：近年研究表明，PI3K/Akt／mTOR信号转导通路是细胞内重要的信号转导通路，脂类激酶PBK和它的下游靶点Akt，即蛋白激酶B，在各种酪氨酸激酶受体诱导的致癌信号通路中发挥了重要的作用。PBK／Akt信号通路的成分在人类大多数恶性肿瘤中都发生了改变，尤其在卡波肉瘤的增殖、存活和抵抗凋亡、血管发生中发挥了重要作用。人类8型疱疹病毒（HHV-8）可通过激活PBK-Akt／PKB／mTOR信号转导通路抑制感染细胞的凋亡，从而维持病毒在人体内的感染和生存。本文就HHV-8与PBK-Akt／PKB信号转导通路的关系及在卡波肉瘤发生、发展中的可能机制作一综述。The phosphatidylinositol 3- kinase-Akt/PKB （PI-3K-Akt/PKB） signal transduetion path- way has become recognized as an important factor. The lipid kinase phosphoinositied 3-OH kinase （PI3K） and its downstream target Akt, that is protein kinase B （PKB）, plays important roles in carcinogenesis sig- nal pathway reduced by kinds of PTK receptor. The component of PI3K/Akt in many malignant tumors in human has changed, which plays an important role especially in the proliferation, survival, anti apoptosis, vasculogenesis of kaposi＇s sarcoma. The kaposi＇s sarcoma-associated herpesvirus （HHV-8） may prevents virally infected cells from undergoing apoptosis, maintains infected cell survival and the virus infection through the phosphatidylinositol 3 ＇-kinase/Akt signal transduction pathway. This paper reviewed the relationship of HHV-8 and PI3K/Akt/mTOR signaling pathway. And further discuss their possible mechanisms in kaposi＇s sareomagenesis.

关 键 词：人类8型疱疹病毒 PI3K/Akt/mTOR信号转导通路 卡波肉瘤 

分 类 号：R373.11[医药卫生—病原生物学]