The role of Fas/Fas ligand system in human

Fas/APO-1（CD 95）是一种细胞表面受体，当它与Fas配体（FasL）或Fas抗体反应时介导凋亡。我以前报道过Fas主要在坏死周围胶质瘤细胞中诱导表达，这表明Fas诱导与凋亡和坏死形成相关，这是胶质母细胞瘤的组织学标志。半胱天冬酶家族的半胱氨酸蛋白酶{白细胞介素-1 β-转化酶（ICE）}已经被认为是细胞死亡途径的组分，并且已经被报道参与Fas、化疗剂和辐射诱导的细胞凋亡。在这项研究中，我评估了表达的FasL，ICE，ICE/CED-3同源-IL（ICH-1），和CPP 32/Yama/apopain在13例原发性星形细胞脑肿瘤（2低级别星形细胞瘤，5间变性星形细胞瘤，6胶质母细胞瘤）通过逆转录（RT）-PCR，蛋白质印迹分析，免疫组化。RT-PCR结果显示所有星形胶质细胞瘤均表达FasL，免疫组化显示FasL主要表达于胶质瘤细胞的质膜上。这些结果表明，FasL的表达是常见的人星形胶质细胞脑肿瘤，并可能导致胶质瘤细胞凋亡，如果诱导Fas表达。ICE、ICH-1和CPP 32过表达的频率似乎与星形细胞脑肿瘤的恶性程度相关。此外，ICH-1和CPP 32过表达可能在坏死的发病机制中发挥重要作用，坏死是胶质母细胞瘤的组织学标志之一。

Fas/APO-1 (CD95) is a cell surface receptor that mediates apoptosis when it reacts with Fas ligand (FasL) or Fas antibody. I previously reported that Fas expression in predominantly induced in perinecrotic glioma cells, suggesting that Fas induction is associated with apoptosis and necrosis formation, a histological hallmark of glioblastomas. Cysteine proteases of caspase family {interleukin-1 beta-converting enzyme (ICE)} have been implicated as components of cell death pathway and have been reported to involved in Fas, chemotherapeutic agents, and radiation-induced apoptosis. In this study, I assessed the expression lf FasL,ICE,ICE/CED-3 homologue-IL (ICH-1), and CPP32/Yama/apopain in 13 cases of primary astrocytic brain tumors (two low grade astrocytomas, five anaplastic astrocytomas, and six glioblastomas) by reverse transcription (RT) -PCR,Western blot analysis, and immunohistochemistry. RT-PCR revealed that all astrocytic brain tumors express FasL.Immunohistochemically, FasL was predominantly expressed on the plasma membrane of glioma cells. These results suggest that FasL expression is common in human astrocytic brain tumors and may cause apoptosis of glioma cells if Fas expression is induced. The frequency of ICE,ICH-1, and CPP32 overexpression appears to correlate with the malignacy grade of astrocytic brain tumors. Furthermore, ICH-1 and CPP32 overexpression may play an important role in the pathogenesis of necrosis, which is one of the histological hallmarks of glioblastoma.