首页> 外文会议>The 6th International Conference on Biomedical Engineering and Rehabilitation Engineering (ICBME '2002) May 27-30, 2002 Guilin, China >DYSREGULATION OF THE RAS-ONCOGENE AND P53 TUMOUR SUPPESSOR GENE EXPRESSION IN THE POLYURETHANE INDUCED TUMOUR CELL LINES IN VITRO
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DYSREGULATION OF THE RAS-ONCOGENE AND P53 TUMOUR SUPPESSOR GENE EXPRESSION IN THE POLYURETHANE INDUCED TUMOUR CELL LINES IN VITRO

机译:聚氨酯诱导的肿瘤细胞株中RAS癌基因和P53肿瘤支持基因的表达失调

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The polyurethanes (PUs) in vitro induced tumor cell clones, namely, clone-2, 5 and 6, isolated from mouse Balb/c3T3 (A311) were further analysized the p21-ras-protein and p53 protein expression and the N, K, H-ras proto-oncogene and p53 tumor suppressor gene exon 5,6,7,8 sequence. Our experimental results shown that the tumor clones increase the ras-protein expression comparing with the untransformed control cell A3111. The tumor clones also slightly increase (p 0.05, only clone 2 p 0.05) the accumulation of p53 inside the cells comparing with A3111. No mutation were detected in the codon 12, 13 and 61 of N, K, H-ras proto-oncogene and p53 tumor suppressor gene exon 5, 6, 7 and 8. The results indicated that PUs induced tumors do not cause the ras-proto-oncogene and the p53 tumor suppressor gene mutation, therefore, the leachable substances of PUs come into the cells or through the signal pathway by the interaction between PUs surfaces and the cells cause the overexpression of the ras-protein and the p53. The ras-protein as a signal protein bound to GTP forming a P21-ras-GTP complex and transfer the signal to the nucleus, cause the cells to be tumorigenic and overproliferation.
机译:从小鼠Balb / c3T3(A311)中分离出的聚氨酯(PU)体外诱导的肿瘤细胞克隆,即克隆2、5和6,进一步分析了p21-ras-蛋白和p53蛋白的表达以及N,K, H-ras原癌基因和p53抑癌基因外显子5、6、7、8的序列。我们的实验结果表明,与未转化的对照细胞A3111相比,肿瘤克隆增加了ras蛋白的表达。与A3111相比,肿瘤克隆在细胞内的p53积累也略有增加(p 0.05,仅克隆2 p 0.05)。在N,K,H-ras原癌基因和p53抑癌基因外显子5、6、7和8的密码子12、13和61中未检测到突变。结果表明PU诱导的肿瘤不会引起ras-因此,由于原癌基因和p53抑癌基因突变,PU的可浸出物质通过PU表面与细胞之间的相互作用进入细胞或通过信号途径进入细胞,导致ras蛋白和p53的过表达。作为信号蛋白的ras蛋白与GTP结合,形成P21-ras-GTP复合物,并将信号转移到细胞核,导致细胞致瘤和过度增殖。

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