抗癌药物与肿瘤细胞膜PI激酶活性关系研究  

Relationship of antitumor durgs and tumor cellmembrane phoshpatidylinositol kinase

作　　者：梁谋[1] 吴波[1] 梁念慈[1] 

机构地区：[1]广东医学院病理生理教研室,广东医学院病理生化教研室,深圳三九企业集团医药研究院

出　　处：《中国药理学通报》1994年第1期60-63,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目

摘　　要：研究临床常用的８种抗癌药物对人慢性骨髓性白血病Ｋ５６２细胞增殖和细胞膜磷脂酰肌醇激酶活性的影响，发现通过抑制细胞核酸或蛋白质代谢而起作用的５－氟脲嘧啶、氨甲喋呤、多粘菌素Ｂ、高三尖杉酯碱及长春新碱在明显抑制细胞增殖的同时显著降低ＰＩ激酶活性，提示降低ＰＩ激酶活性是它们影响细胞核酸或蛋白质代谢，进而抑制细胞增殖的早期生化过程之一。与之相反．强烈抑制Ｋ５６２细胞增殖．直接作用于ＤＮＡ的阿霉素与烷化剂噻替派、环磷酰胺一样．并不影响ＰＩ激酶活性．表明它们的抗癌机理不涉及细胞膜ＰＩ激酶活性的变化。Effects of eight antitumor drugs on cell proliferation and cell membrane phosphatidylinositol(PI)kinase in human chronic myelogenous Leukemia K562 cells were studied.The results indicated that 5-flurouracil,methotrexate, polymyxin B, homoharringtonine and vincristine not only inhibited obviously the cell proliferation but also sigflificantly decreased the activity of PI kinases, it suggests that the decrease of PI kinase acitity is one of initianl processes that affact the metabolism of nucleal acid ar protein, and then inhibit cell proliferation. on the contrary, adriamycin that obviously inhibits K562 cell proliferation, same as thiotepa and cytoxan that act directly on DNA,don't affact the P1 kinase activitty, which suggests that their mechanism of antitumor has nothing to do with the change of PI kinase.

关 键 词：白血病 细胞增殖 抗癌药 

分 类 号：R966[医药卫生—药理学]