中文摘要：

背景与目的：辐射致癌的机制目前尚不明确。本研究通过建立辐射致癌的细胞模型,应用蛋白质组学技术观察辐射癌变细胞和正常细胞间的差异蛋白表达谱,以期获得辐射致癌相关蛋白。方法：选取永生化的人支气管上皮细胞株（BEAS-2B）,利用γ射线照射诱导癌变,建立辐射致癌的细胞模型。利用二维凝胶电泳技术,筛选癌变细胞和正常细胞间的差异表达蛋白点并进行质谱鉴定分析。通过Western blot技术对其中4个蛋白：ENO1、PrxⅠ、Dyrk2和GPX1在辐射致癌不同阶段的表达情况进行分析。结果：在辐射癌变细胞和正常细胞间共得到可信差异表达蛋白点59个。其中14个仅在癌变细胞中表达,15个仅在正常细胞中表达,23个在癌变细胞中表达降低,7个在癌变细胞中表达升高。通过质谱分析,共有26个蛋白点得到鉴定,主要包括一些参与细胞代谢、增殖、分化的酶类、信号调控蛋白、DNA结合蛋白以及一些细胞结构蛋白和少数功能不明的蛋白及肽段。其中ENO1和PrxⅠ随辐射癌变的进展而升高,Dyrk2和GPX1随辐射癌变的进展而降低。结论：应用二维电泳技术可获得辐射致癌差异表达蛋白谱,筛选和鉴定出与辐射致癌相关的差异表达蛋白,并可检测部分差异蛋白在辐射致癌不同阶段的表达情况。

英文摘要：

BACKGROUND ＆ OBJECTIVE. Carcinogenesis is the most serious late effect of radiation, but the mechanism of radiation-induced carcinogenesis remains unknown. This study was to compare the protein expression profiles between radiation-induced cancer cells and normal cells. METHODS： Immortalized human bronchia endothelial cell line BEAS-2B was irradiated by γ-ray to prepare malignant BR22P50 cells. Protein profiles of BR22P50 cells and normal cell line BNP50 were detected by two-dimensional （2D） electrophoresis. The differentially expressed proteins were identified by mass spectrometry. The protein levels of ENO1, PrxⅠ, Dyrk2, and GPX1 in different phases of radiation-induced carcinogenesis were detected by Western blot. RESULTS. A total of 59 proteins were differentially expressed between BR22P50 and BNP50 cells. Of the 59 proteins, 14 were only expressed in BR22P50 cells, 15 were only expressed in BNP50, 7 were overexpressed and 23 were lowly expressed in BR22P50 cells. Using MALDI-TOF MS technology, 26 proteins were identified, including enzymes, structure proteins, cell signal proteins, binding proteins, metabolism-related proteins, some unknown functional proteins, and poly-peptides. The expression of ENO1 and PrxⅠ was up-regulated and that of Dyrk2 and GPX1 was down-regulated with the advancement of radiation-induced carcinogenesis. CONCLUSIONS; The proteins related to radiation-induced carcinogenesis are identified by 2D electrophoresis. This study may provide a novel clue to probe the mechanism of radiation-induced carcinogenesis.