现代肿瘤医学
現代腫瘤醫學
현대종류의학
JOURNAL OF MODERN ONCOLOGY
2009年
8期
1432-1434
,共3页
肝细胞癌%血管内皮生长因子%磷脂酰肌醇3-激酶
肝細胞癌%血管內皮生長因子%燐脂酰肌醇3-激酶
간세포암%혈관내피생장인자%린지선기순3-격매
hepatocellular carcinoma%vascular endothelial growth factor%phosphatidylinositol 3-kinase
目的:研究磷脂酰肌醇3-激酶(PI3K)信号通路在肝癌细胞血管内皮生长因子(VEGF)表达调控中的作用.方法: 体外培养高转移性人肝癌细胞株HCCLM3,分为对照组、PI3K特异性抑制剂LY294002浓度5μmol/L组,LY294002浓度10μmol/L及20μmol/L组,处理6小时后,采用逆转录聚合酶链反应(RT-PCR)技术检测VEGF mRNA表达的变化.结果: LY294002可使肝癌细胞HCCLM3的VEGF mRNA的表达下降,且这种抑制作用随着LY294002浓度增大而增大(P<0.01),呈现剂量移赖性关系.结论: LY294002可以抑制肝癌细胞株HCCLM3中VEGF的表达,肝癌细胞VEGF的表达调控受PI3K信号通路调控.
目的:研究燐脂酰肌醇3-激酶(PI3K)信號通路在肝癌細胞血管內皮生長因子(VEGF)錶達調控中的作用.方法: 體外培養高轉移性人肝癌細胞株HCCLM3,分為對照組、PI3K特異性抑製劑LY294002濃度5μmol/L組,LY294002濃度10μmol/L及20μmol/L組,處理6小時後,採用逆轉錄聚閤酶鏈反應(RT-PCR)技術檢測VEGF mRNA錶達的變化.結果: LY294002可使肝癌細胞HCCLM3的VEGF mRNA的錶達下降,且這種抑製作用隨著LY294002濃度增大而增大(P<0.01),呈現劑量移賴性關繫.結論: LY294002可以抑製肝癌細胞株HCCLM3中VEGF的錶達,肝癌細胞VEGF的錶達調控受PI3K信號通路調控.
목적:연구린지선기순3-격매(PI3K)신호통로재간암세포혈관내피생장인자(VEGF)표체조공중적작용.방법: 체외배양고전이성인간암세포주HCCLM3,분위대조조、PI3K특이성억제제LY294002농도5μmol/L조,LY294002농도10μmol/L급20μmol/L조,처리6소시후,채용역전록취합매련반응(RT-PCR)기술검측VEGF mRNA표체적변화.결과: LY294002가사간암세포HCCLM3적VEGF mRNA적표체하강,차저충억제작용수착LY294002농도증대이증대(P<0.01),정현제량이뢰성관계.결론: LY294002가이억제간암세포주HCCLM3중VEGF적표체,간암세포VEGF적표체조공수PI3K신호통로조공.
Objective:To investigate the roles of phosphatidylinositol 3-kinase(PI3K) in the regulation of expression of vascular endothelial growth factor(VEGF) in hepatocellular carcinoma(HCC) cells. Methods: The high metastasic cell line HCCLM3 were cultured in DMEM medium,HCCLM3 cells were divided into control groups and LY294002 groups(5μM,10μM,20μM),LY294002 was the specific inhibitor of PI3K.The expression of VEGF mRNA was detected by reverse transcriptional polymerase chain reaction(RT-PCR) after 6 hours. Results: In HCCLM3 cells,the expression of VEGF mRNA can be apparently inhibited by LY294002. With the increase of LY294002 concentration,the expression of VEGF mRNA decreased gradually(P<0.01)and in a dose-dependent manner. Conclusion: LY294002 can reduce the expression of VEGF mRNA in HCCLM3 cell line,the expression of VEGF in HCC cells is regulated by PI3K.