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目的 检测肾细胞癌 (RCC)组织脆性组氨酸三联体 (fragilehistidinetraid ,FHIT)基因蛋白编码外显子及mRNA表达情况 ,了解RCC组织中FHIT基因异常特征 ,探讨FHIT基因与RCC发生发展的关系。方法 收集RCC及相应癌周肾组织标本 ,提取组织DNA及RNA。DIG标记FHIT全长cDNA探针。PCR法扩增FHIT基因E5～E9。扩增产物电泳转膜后行Southernblot杂交。RNA转膜后行Northernbolt杂交。结果 6 8.2 %(1 5 / 2 2 )RCC组织、37.5 % (6 / 1 4 )相应癌周肾组织存在FHIT基因蛋白编码外显子缺失或异常。E5和E8异常(缺失、突变等 )发生率为 40 .9% (9/ 2 2 )和 36 .4% (8/ 2 2 )。 42 .8% (1 2 / 2 8)RCC及 75 % (1 2 / 1 6 )癌周肾组织存在Northernblot阳性条带。FHITmRNA失表达与RCC组织学高分级及临床高分期关系密切 (P <0 .0 5 )。存在FHIT基因蛋白编码外显子缺失或异常的 1 5例RCC中 1 4例 (93.3% )FHIT基因mRNA表达阴性。结论 RCC组织常发生FHIT基因蛋白编码外显子缺失或突变。FHITmRNA失表达与FHIT基因异常基本一致 ,其表达情况可提示患者预后。本实验结果支持FHIT基因可能是肿瘤抑制基因
Objective To detect the expression of exon and mRNA of fragile histidinetraid (FHIT) gene in renal cell carcinoma (RCC) tissues and to investigate the abnormality of FHIT gene in RCC tissues and to explore the relationship between FHIT gene and the occurrence and development of RCC. Methods RCC and corresponding peritumoral kidney tissue samples were collected and tissue DNA and RNA were extracted. DIG-labeled FHIT full-length cDNA probe. PCR amplification of FHIT gene E5 ~ E9. Amplification products were electrophoresed and Southernblot hybridization was performed. Transfection of RNA Northernbolt hybridization. Results There was a deletion or abnormality of coding exon of FHIT gene in 6 8.2% (15/2) RCC tissues and 37.5% (6/1 4) corresponding perineurial neoplasms. The incidences of E5 and E8 abnormalities (deletion, mutation, etc.) were 40.9% (9/2 2) and 36.4% (8/2 2). There were Northern blot positive bands in 42.8% (1 2/2 8) RCC and 75% (1 2/1 6) peritumoral nephridial tissues. FHIT mRNA loss of expression and RCC histological high grade and clinical stage (P <0.05). 14 (93.3%) of FHIT gene mRNAs were negative in 15 RCCs with deletion or abnormality of exon encoding FHIT gene protein. Conclusion The deletion or mutation of FHIT gene encoding exon in RCC tissues often occurs. FHIT mRNA loss of expression and FHIT gene abnormalities are basically the same, the expression of the situation can prompt the prognosis of patients. Our results support FHIT gene may be tumor suppressor gene