受辐射肝癌细胞所诱导旁效应与p53的关系  

Relationship between P53 and bystander effect Induced by radiated hepatoma cells

作　　者：赵镁嘉[1] 沈波[1] 袁德晓[1] 陈红红[1] 邵春林[1] 

机构地区：[1]复旦大学放射医学研究所,上海200032

出　　处：《核技术》2009年第6期469-472,共4页Nuclear Techniques

基　　金：国家自然科学基金(30670629;30770644);教育部新世纪优秀人才支持计划(NCET-06-0365);上海市浦江人才计划(06PJ14012)项目资助

摘　　要：通过检测受照射细胞及与其共培养旁细胞的损伤情况及p53抑制剂对其的影响,研究了肝癌细胞辐射敏感性及辐射诱导的旁效应与p53的关系。发现肝癌细胞的辐射敏感性与p53密切相关:野生型p53辐射敏感性最高,突变型的次之,缺失型的敏感性最低。同时,辐射诱导的旁效应与p53状态亦密切相关,仅野生型p53肝癌细胞(HepG2)对旁细胞(Chang氏肝细胞)具有旁效应,且未受照射旁细胞中产生的微核具有明显的剂量效应和时间效应;而突变型(PLC)和缺失型(Hep3B)的肝癌细胞几乎不能诱导辐射旁效应的产生。另外,p53抑制剂可显著抑制辐射旁效应的产生。The role of p53 in bystander responses on normal liver cells were investigated by co-culturing irradiated hepatoma cells with non-irradiated bystander Chang liver cells. It was found that radiosensitivity of the hepatoma cells was relative to p53. HepG2 cells with wtp53 had the highest radiosensitivity followed by PLC/PRF/5 cells with mtp53 and Hep3B cells with null-p53. The induction of bystander micronucleus （MN） was observed only in the Chang liver cells that had been co-cultured with HepG2 cells but not co-cultured with PLC/PRF/5 or Hep3B. Also, this bystander MN was relative to the irradiation dose and the cell co-culture rime. When the hepatoma cells were treated with pifithfin-α, a p53 inhibitor, their radiosensitivities were reduced, and the bystander effect was diminished. The results indicate that p53 could regulate not only the radiosensitivity but also the bystander response.

关 键 词：肝癌细胞 辐射敏感性 旁效应 P53 

分 类 号：Q691.5[生物学—生物物理学] R811.5[医药卫生—放射医学]