Small interfering RNA targeting to hepatitis B virus X gene and 5-aza-2'-deoxycytidineon inhibite growth of the subcutaneous implanted tumor of hepatocellular carcinoma in nude mice
10.3760/cma.j.issn.1003-9279.2012.05.013
- VernacularTitle:HBV X siRNA与5-氮-2'-脱氧胞苷对裸鼠肝癌皮下移植瘤作用的研究
- Author:
Li MAI
1
;
Lin YANG
;
Jian-Yu KUANG
;
Shao-Quan ZHANG
;
Yan-Hong KANG
;
Qi-Huan XU
;
Qi-Feng XIE
Author Information
1. 中山大学附属第三医院感染病科
- Keywords:
Hepatitis B virus;
DNA;
RNA;
Liver neoplasms;
Carcinoma hepatocellular
- From:
Chinese Journal of Experimental and Clinical Virology
2012;26(5):362-365
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the anti-tumor effect of small interfering RNA targeting to HBV X gene (X-siRNA) and 5-aza-2'-deoxycytidine (5-aza-dC) on HBV-related hepatocellular carcinoma.Methods X-siRNA and control siRNA were synthesized.HepG2/GFP-HBx cells were treated with X-siRNA,and the levels of HBV X mRNA were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).Nude mice were inoculated with HepG2/GFP and HepG2/GFP-HBx cells subcutaneous respectively to establish implant models of hepatocellular carcinoma,and were treated with X-siRNA,5-aza-dC alone or in combination,and tumor growth was observed.The methylation of p16 gene promoter was detected by methylation specific polymerase chain reaction (MSP).Results RT-PCR showed the expression of HBV X mRNA in HepG2/GFP-HBx cells was inhibited markedly by X-siRNA.The nude mice experiment showed that the gross tumor volume was much bigger in HepG2/GFP-HBx group than that in HepG2/GFP group (P ＜ 0.05).The growth of palpable tumors in X-siRNA or 5-aza-dC treatment group notably decreased (P ＜ 0.05).MSP analysis showed that p16 gene methylation was observed in HepG2/GFP-HBx-caused palpable tumors,while no methylation was detected in HepG2/GFP group.However,after treatment with X-siRNA or 5-aza-dC,p16 gene methylation reduced.Conclusions HBV X-siRNA and methylation inhibitor can inhibit the growth of hepatoma cells via reversing p16 methylation.
