摘要
目的:对采用人类全基因组芯片检测到的甲基丙烯酸环氧丙酯(glycidylmethacrylate,GMA)致人支气管上皮(16HBE)细胞恶性转化过程中差异基因进一步进行其表达改变的研究。方法:采用实时定量PCR技术分析GMA诱导16HBE细胞恶性转化过程中,第10代(转化前期)和第30代(转化后期)细胞的信号转导和有丝分裂相关基因C19orf20、RGS14、EPB49、PSCA、CENPF、CTGF、RASD1的表达。结果:C19orf20、RGS14基因在转化前期细胞中表达分别上调421%、178%;CENPF、CTGF基因在转化后期细胞中表达分别下调93%、77%;EPB49基因在转化前期、转化后期细胞中表达分别上调191%、116%;PSCA基因在转化前期、转化后期细胞中表达分别上调593%、119%;RASD1基因在转化前期细胞中表达上调231%,而在转化后期细胞中表达下调74%。结论:GMA致16HBE细胞恶性转化过程是涉及多基因共同作用的复杂过程,C19orf20、RGS14、EPB49、PSCA、CENPF、CTGF、RASD1基因的异常表达可能在该过程中起着重要作用。
OBJECTIVE:To examine the expression of relative genes,screened by gene chip,in transformation of human bronchial epithelial cells induced by glycidyl methacrylate.METHODS:Real time polymerase chain reaction was used to measure the expression of C19orf20,RGS14,EPB49,PSCA,CENPF,CTGF and RASD1,involving in mitosis and signal transduction,in transformation of human bronchial epithelial cells induced by glycidyl methacrylate.RESULTS:Expressions of C19orf20 and RGS14 were up-regulated by 421% and 178%,respectively,in the transformed 10th-generation(protophase)cells.CENPF and CTGF were down-regulated by 93% and 77%,respectively,in the transformed 30th-generation(anaphase)cells.EPB49 and PSCA were up-regulated by 191% and 593%,respectively,in the malignant transformation protophase cells,and by 116% and 119%,respectively,in the malignant transformation anaphase cells.RASD1 expression was 231% up-regulated in the malignant transformation protophase cells while 74% down-regulated in the malignant transformation anaphase cells.CONCLUSION:The malignant transformation of human bronchial epithelial cells is a complicated process involving many genes.The alteration of the above genes may be important molecular events during the transformation of human bronchial epithelial cells induced by glycidyl methacrylate.
出处
《癌变.畸变.突变》
CAS
CSCD
2010年第4期249-254,共6页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家自然科学基金资助项目(30671789)
关键词
甲基丙烯酸环氧丙酯
人支气管上皮细胞
恶性转化
基因表达
glycidyl methacrylate
human bronchial epithelial cells
malignant transformation
gene expression.