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1.
Chinese Journal of Digestive Surgery ; (12): 666-670, 2014.
Article in Chinese | WPRIM | ID: wpr-455358

ABSTRACT

Liver cancer is one of the most common malignant tumors in China.The efficacy of traditional treatment for liver cancer is unsatisfactory,and the prognosis of the patients is poor.In recent 10 years,with the development of the molecular biological techniques,genetic therapy has become a new and promising approach for liver cancer.Of which,adenovirus mediated herpes simplex virus thymidine kinase (ADV-tk) for the treatment of liver cancer is widely applied.The enzyme secreted by ADV-tk transformed the prodrug gancyclovir (GCV) to the cytotoxic agents and thus to kill the liver cancer cells.The results of multiple animal and clinical experiments showed that ADV-tk/GCV is effective for the treatment of liver cancer.In this article,the recent progress of ADV-tk/GCV in the treatment of liver cancer was reviewed.

2.
Academic Journal of Second Military Medical University ; (12): 1109-1112, 2010.
Article in Chinese | WPRIM | ID: wpr-841039

ABSTRACT

Objective: To study the inhibitory effects of an adenovirus (Ad)-based short hairpin RNA (shRNA) expression system on expression of vascular endothelial growth factor receptor (VEGFR) and on growth of colon carcinoma cells in vitro and in vivo. Methods: RNA interference pAd-Easy/VEGFR vector was used to transfect 293 cells via Lipofectamine 2000. The adenoviral vector carrying VEGFR was used to transfect CW2 cells and the transfection efficiency was determined by fluorescent microscope and flow cytometry. The expression of VEGFR was examined by RT-PCR and Western blotting. The cell growth was observed with MTT method and the growth curve was plotted. Nude mouse was transplanted with CW2 cells to establish colon cancer tumor model and the growth of tumor was observed daily. Micro-vessel density (MVD) was detected by immunohistochemistry. Results: The recombinant pAd-Easy carrying shRNA against VEGFR was verified by sequencing. Flow cytometry showed that the transfection efficiency of CW2 cells was 99.7%. RT-PCR and Western blotting showed that the expression of VEGFR in pAd-Easy/VEGFR group was obviously decreased. The growth curve showed that the cell growth in the pAd-Easy/ VEGFR group was obviously slowed down. We also found that the tumor growth in the nude mouse model was obviously inhibited and the MVD was also decreased. Conclusion: pAd-Easy/VEGFR-mediated VEGFR shRNA can effectively inhibit the expression of VEGFR in CW2 cells and suppress tumor growth in vivo.

3.
Academic Journal of Second Military Medical University ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-562356

ABSTRACT

Objective:To study the inhibitory effects of an adenovirus(Ad)-based short hairpin RNA(shRNA) expression system on expression of vascular endothelial growth factor receptor(VEGFR) and on growth of colon carcinoma cells in vitro and in vivo.Methods: RNA interference pAd-Easy/VEGFR vector was used to transfect 293 cells via Lipofectamine 2000.The adenoviral vector carrying VEGFR was used to transfect CW2 cells and the transfection efficiency was determined by fluorescent microscope and flow cytometry.The expression of VEGFR was examined by RT-PCR and Western blotting.The cell growth was observed with MTT method and the growth curve was plotted.Nude mouse was transplanted with CW2 cells to establish colon cancer tumor model and the growth of tumor was observed daily.Micro-vessel density(MVD) was detected by immunohistochemistry.Results: The recombinant pAd-Easy carrying shRNA against VEGFR was verified by sequencing.Flow cytometry showed that the transfection efficiency of CW2 cells was 99.7%.RT-PCR and Western blotting showed that the expression of VEGFR in pAd-Easy/VEGFR group was obviously decreased.The growth curve showed that the cell growth in the pAd-Easy/VEGFR group was obviously slowed down.We also found that the tumor growth in the nude mouse model was obviously inhibited and the MVD was also decreased.Conclusion: pAd-Easy/VEGFR-mediated VEGFR shRNA can effectively inhibit the expression of VEGFR in CW2 cells and suppress tumor growth in vivo.

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