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作 者:闵红波[1] 黄勤[2] 王建文[3] 孙继虎[3] 步世忠[3]
机构地区:[1]解放军第455医院眼科,上海200052 [2]第二军医大学附属长海医院内分泌科,上海200433 [3]第二军医大学生理学教研室,上海200433
出 处:《中国癌症杂志》2004年第6期510-512,516,共4页China Oncology
摘 要:目的 :研究紫杉醇 (Tax)抑制视网膜母细胞瘤 (Rb)细胞生长并诱导其凋亡及磷酸化Bcl 2在其中的作用。方法 :应用3 H 胸腺嘧啶掺入分析法观察Tax对细胞生长的抑制作用 ,以DNA片段凝胶电泳分析细胞凋亡 ,用Westernblot分析Tax对磷酸化Bcl 2的影响 ,用cDNA细胞转染法观察突变型Bcl 2阻断Tax的作用。结果 :Tax可明显地抑制Y79细胞的生长 ,1μmol/LTax处理 2 4小时 ,3 H 胸腺嘧啶掺入率下降达 5 5 .4 3% ,Tax可诱导Y79细胞凋亡。在此过程中 ,Bcl 2被磷酸化。当Y79细胞被转染突变型Bcl 2后 ,Tax对Y79细胞的作用被阻断。结论 :Tax可抑制Y79细胞生长并诱导其凋亡 ,磷酸化Bcl 2参与其过程。Purpose:To investigate palitaxel (Tax) induct io n of apoptosis in human retinoblastoma Y79 cells and the role of Bcl-2 phosphor ylation in the mechanism. Methods:Antiproliferation effects of Tax on Y79 cells were dete rmined by 3H-thymidine incorporation. Apoptosis of the Tax-treated cells was determined by DNA fragmentation analysis. Bcl-2 phosphorylation was determ ined by Western blot analysis. Cell transfection was used in mutant Bcl-2 trans fecting in Y79 cells. Results:After 24 hours treatment with 1 μmol/L Tax, 3H- thymidine incorporation decreased in Y79 cells and the effects were time and dos e dependent. DNA ladder appeared in DNA fragmantation analysis after 12-24 hour s treatment with Tax. Bcl-2 Phosphorylation was significantly increased in 12- 24 hours treatment with Tax. Bcl-2, a mutant of Bcl-2, blocked Tax activation process. Conclusions:Tax inhibits cell growth and induces apoptosis in h uman Y79 cells, and phosphorylation of Bcl-2 might be involved in this process.
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