These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Hepatitis B virus X protein activates expression of IGF-IR and VEGF in hepatocellular carcinoma cells].
    Author: Tao X, Shen D, Ren H, Zhang X, Zhang D, Ye J, Gu B.
    Journal: Zhonghua Gan Zang Bing Za Zhi; 2000 Jun; 8(3):161-3. PubMed ID: 10880166.
    Abstract:
    OBJECTIVE: The expression of insulin-like growth factor I receptor (IGF-IR) and the vascular endothelial growth factor (VEGF) in HepG(2) 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 HepG(2) cells. The modified cell HepaG(2)-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%A3% in the transfected HBx gene cells, 26%A4% in X(0) control cells. The positive rate of VEGF expressed x cells was 83%A5%, X(0) cells was 28%A6% (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 X(0) 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.
    [Abstract] [Full Text] [Related] [New Search]