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作 者:赵燕颖[1] 李亚刚[1] 颜波群[1] 刘志忠[1] 秦国涛[1] 孙远杰[1]
机构地区:[1]吉林大学第四医院消化内科,吉林省长春市130011
出 处:《世界华人消化杂志》2016年第3期355-361,共7页World Chinese Journal of Digestology
基 金:吉林省卫生厅基金(青年基金)资助项目;No.2013Q024~~
摘 要:目的:研究血管内皮生长因子165b(vascular endothelial growth factor 165b,VEGF165b)在肝细胞癌和正常肝组织中的表达情况,初步探讨其与肝细胞癌的关系和作用机制.方法:用免疫组织化学法检测28例肝细胞癌组织和30例正常肝组织中VEGF165b蛋白的表达情况;用RT-PCR法分别检测肝细胞癌和正常肝组织中VEGF165b和VEGF165 mRNA的表达情况.用Western blot法检测上述肝细胞癌组织和正常肝组织中VEGF165b和VEGF165蛋白的表达情况.用Western blot法检测上述肝细胞癌和正常肝组织中FAK和P-Akt蛋白的表达情况.结果:正常肝脏组织中VEGF165b蛋白表达率为96.67%(29/30),肝细胞癌组织中VEGF165b蛋白的表达率为21.4%(6/28),表达差异有统计学意义(P<0.05).VEGF165b mRNA和蛋白在肝癌组织中的表达明显低于正常肝脏组织的表达(P<0.01).VEGF165 mRNA和蛋白在肝癌组织中的表达明显高于正常肝脏组织的表达(P<0.01).FAK和P-Akt蛋白在肝癌组织中的表达明显高于正常肝脏组织的表达(P<0.01).结论:VEGF165b在肝细胞癌组织中的表达明显低于正常肝组织的表达,而VEGF165和FAK、P-Akt在肝细胞癌组织中的表达明显高于正常肝组织的表达.提示VEGF165b与肝癌发生、发展有关,其机制可能是VEGF165b抑制VEGF165、FAK和P-Akt表达及他们的促进血管生成、肿瘤生长作用.AIM: To detect the expression of vascular endothelial growth factor 165b(VEGF165b) in hepatocellular carcinoma(HCC), and to investigate the relationship between VEGF165 b and HCC.METHODS: Expression of VEGF165 b protein in 28 HCC specimens and 30 normal liver tissue specimens was detected by immunohistochemistry. The expression of VEGF165 and VEGF165 b mRNAs was detected by RT-PCR. The expression of VEGF165, VEGF165 b, FAK and P-Akt proteins in HCC and normal liver tissues was detected by Western blot.RESULTS: The positive rate of VEGF165 b protein expression in normal liver tissues was significantly higher than that in HCC tissues [96.67%(29/30) vs 21.4%(6/28), P〈0.05]. VEGF165 b mRNA and protein expression in HCC tissues was significantly lower than that in normal liver tissues(P〈0.01). The expression of VEGF165 mRNA and protein in HCC tissues was significantly higher than that in normal liver tissues(P〈0.01). The expression of FAK and P-Akt proteins in HCC tissues was significantly higher than that in normal liver tissues(P〈0.01).CONCLUSION: The expression of VEGF165 b in HCC tissues is significantly lower than that in normal liver tissues, and the expression of VEGF165, FAK and P-Akt in HCC tissues issignificantly higher than that in normal liver tissues. These findings suggest that VEGF165 b may be related to the occurrence and development of HCC possibly by inhibiting the expression of VEGF165, FAK and P-Akt and their effects on angiogenesis and tumor growth.
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