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肾细胞癌组织与正常组织中VEGF165b的差异表达及其意义 被引量:2

The differential expression of VEGF165b in the renal cell carcinoma and normal renal tissues and its clinical significance
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摘要 目的:研究血管内皮生长因子165b(Vascular endothelial growth factor 165b,VEGF165b)在肾细胞癌(Renalcellcarcino-ma,RCC)组织和正常组织中的表达情况,初步探讨其与肾细胞癌发生发展的关系。方法:(1)用S-P免疫组化法检测30例肾细胞癌组织和29例正常肾组织中VEGF165b蛋白的表达情况;(2)用RT-PCR法分别检测32例肾细胞癌组织和30例正常肾组织中VEGF165b mRNA的表达情况。结果:(1)正常肾组织中VEGF165b蛋白表达率为96.55%(28/29),肾细胞癌组织中VEGF165b蛋白的表达率为20.00%(6/30),表达差异有统计学意义(P<0.05)。(2)正常肾组织中VEGF165b mRNA阳性表达率为93.33%(28/30),肾细胞癌组织中VEGF165b mRNA的阳性表达率为18.75%(6/32),具有统计学意义(P<0.05)。结论:VEGF165b在肾细胞癌组织中的表达低于正常肾组织的表达,这种表达差异可能与肾癌发生、发展的机制有关。 Objective: To investigate the differential expression of VEGF165b in the renal cell carcinoma (RCC) and normal renal tissues and its role in the development of RCC. Methods: S-P immunohistochemistry was used to detect the expression of VEGF165b protein in 30 specimens of paraffin-embedded RCC tissues and 29 specimens of paraffin-embedded normal renal tissues. RT-PCR was performed to detect the expression of VEGF165b mRNA in 32 specimens of fresh RCC tissues and 30 specimens of fresh normal renal tissues. Results: Among 29 of normal renal tissues, 28 specimens had positive expression of VEGF165b protein, with the positive rate of 96.55% (28/29) that was significantly higher than 20.00% (6/30)in RCC tissues (P〈0.05). The positive rate of VEGF165b mRNA in normal renal tissues was 93.33%(28/30) ,while that of RCC tissues was only 18.75% (6/32). The positive expression rate of VEGFI65b mRNA in RCC tissues was significantly lower than that in normal renal tissues (P〈0.05). Conclusion: VEGF165b might play a role in inhibiting development of RCC. Vascular endothelial growth factor 165b.
出处 《重庆医科大学学报》 CAS CSCD 北大核心 2009年第3期281-284,共4页 Journal of Chongqing Medical University
基金 重庆市自然科学基金资助项目(CSTC2005BB5033)
关键词 肾肿瘤 VEGF165B 免疫组织化学 逆转录-聚合酶链反应(RT—PCR) Kidney neoplasms Vascular endothelial growth factor 165b Immunohistochemistry Reverse transcriptasc polymerase chain reaction (RT-PCR)
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共引文献6

同被引文献25

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