中华肝脏病杂志
中華肝髒病雜誌
중화간장병잡지
CHINESE JOURNAL OF HEPATOLOGY
2000年
3期
161-163
,共3页
陶小红%张晓实%任红%张大志%叶珈%古柏燕%沈鼎明
陶小紅%張曉實%任紅%張大誌%葉珈%古柏燕%瀋鼎明
도소홍%장효실%임홍%장대지%협가%고백연%침정명
癌,肝细胞%致癌性试验%受体,胰岛素样生长因子-Ⅰ%血管内皮生长因子
癌,肝細胞%緻癌性試驗%受體,胰島素樣生長因子-Ⅰ%血管內皮生長因子
암,간세포%치암성시험%수체,이도소양생장인자-Ⅰ%혈관내피생장인자
Carcinoma,hepatocellular%Carcinogenesis%Receptor,insulin-like growth factor Ⅰ%Vascular endothelial growth factor
目的研究乙型肝炎病毒X(hepatitis B virus,HBx)蛋白对生长因子激活作用,探讨HBx蛋白对肝细胞癌生长的影响。方法构建X基因真核表达载体,转染入HepG2细胞后,细胞组织化学和免疫印迹法检测胰岛素样生长因子-Ⅰ受体(insulin-like growth factor Ⅰreceptor,IGF-ⅠR)和血管内皮生长因子(vascular endothelial growth factor,VEGF)表达。结果转染HBx基因HepG2细胞(X细胞)IGF-ⅠR表达阳性率为84%±3%,转染空载体对照细胞(X0细胞)为26%±4%;免疫印迹法检测X细胞有明显条带。VEGF表达X细胞阳性率为83%±5%,X0细胞为28%±6%,差异有非常显著意义;X细胞IGF-ⅠR表达增高近1.5倍。结论 HBx蛋白可同时激活IGF-ⅠR和VEGF,在肿瘤恶性生长、转移中起有重要作用。
目的研究乙型肝炎病毒X(hepatitis B virus,HBx)蛋白對生長因子激活作用,探討HBx蛋白對肝細胞癌生長的影響。方法構建X基因真覈錶達載體,轉染入HepG2細胞後,細胞組織化學和免疫印跡法檢測胰島素樣生長因子-Ⅰ受體(insulin-like growth factor Ⅰreceptor,IGF-ⅠR)和血管內皮生長因子(vascular endothelial growth factor,VEGF)錶達。結果轉染HBx基因HepG2細胞(X細胞)IGF-ⅠR錶達暘性率為84%±3%,轉染空載體對照細胞(X0細胞)為26%±4%;免疫印跡法檢測X細胞有明顯條帶。VEGF錶達X細胞暘性率為83%±5%,X0細胞為28%±6%,差異有非常顯著意義;X細胞IGF-ⅠR錶達增高近1.5倍。結論 HBx蛋白可同時激活IGF-ⅠR和VEGF,在腫瘤噁性生長、轉移中起有重要作用。
목적연구을형간염병독X(hepatitis B virus,HBx)단백대생장인자격활작용,탐토HBx단백대간세포암생장적영향。방법구건X기인진핵표체재체,전염입HepG2세포후,세포조직화학화면역인적법검측이도소양생장인자-Ⅰ수체(insulin-like growth factor Ⅰreceptor,IGF-ⅠR)화혈관내피생장인자(vascular endothelial growth factor,VEGF)표체。결과전염HBx기인HepG2세포(X세포)IGF-ⅠR표체양성솔위84%±3%,전염공재체대조세포(X0세포)위26%±4%;면역인적법검측X세포유명현조대。VEGF표체X세포양성솔위83%±5%,X0세포위28%±6%,차이유비상현저의의;X세포IGF-ⅠR표체증고근1.5배。결론 HBx단백가동시격활IGF-ⅠR화VEGF,재종류악성생장、전이중기유중요작용。
Objective The expression of insulin-like growth factor Ⅰ receptor(IGF-ⅠR) and the vascular endothelial growth factor(VEGF) in HepG2 cells transfected with a hepatitis B virus X(HBx) expression vector was investigated in an attempt to study their possible relationship to the growth of HBx-induced hepatocellular carcinoma(HCC). Methods The eucaryotic expression vector of HBx gene was constructed and introduced into HepG2 cells. The modified cell HepaG2-X was synchronized in a quiescent state by culture of serum deprivation. The IGF-ⅠR and VEGF were analyzed by immunohistochemical and Western blot technique. Results The positive rate of IGF-ⅠR expression was 84%±3% in the transfected HBx gene cells, 26%±4% in X0 control cells. The positive rate of VEGF expressed x cells was 83%±5%, X0 cells was 28%±6% (P<0.001). The level of IGF-ⅠR and VEGF in serum-starved x modified cells was 1.5 times higher than that of synchronized X0 modified cells. Conclusion Since the IGF-ⅠR is a very important growth factor in sustaining the tumor abnormal growth and the VEGF has a crucial role in inducting tumor angiogenesis, our findings indicate that HBx may play an important role in the processes of HCC by activating IGF-ⅠR and VEGF gene expression.