| 论文题目: | Hepatitis B virus inhibits apoptosis of hepatoma cells by sponging miR-15a/16 cluster |
|---|---|
| 作者: | Liu Ningning, Zhang Jinfang, Jiao Tong, Li Zhiwei, Peng Jirun, Cuizhu Qingqing, Ye Xin* |
| 联系作者: | Ye Xin* |
| 刊物名称: | Journal of Virology |
| 期: | |
| 卷: | |
| 页: | |
| 年份: | 2013 |
| 影响因子: | 4.893 |
| 论文下载: | 下载地址 |
| 摘要: | Hepatitis B virus (HBV) causes chronic hepatitis in hundreds of millions of people worldwide, which can eventually lead to hepatocellular carcinoma (HCC). The molecular mechanisms underlying HBV persistence are not well understood. In this study, we found that HBV inhibited the chemotherapy drug etoposide-induced apoptosis of hepatoma cells. Further analysis revealed that HBV mRNAs possess a miR-15a/16 complementary site (HBV nt1362-1383) acting as sponges to bind and sequester endogenous miR-15a/16. Consequently, the Bcl-2 known as the target of miR-15a/16 was upregulated in HBV infected cells. The data from HBV transgenic mice further confirmed that HBV transcripts cause the reduction of miR-15a/16 and increase of Bcl-2. More importantly, we examined the level of HBV transcripts and miR-15a/16 in HBV-infected HCC from patients and found that the amount of HBV mRNA and the level of miR-15a/16 were negatively correlated. Consistently, the level of Bcl-2 mRNA was upregulated in HBV infected patients. In conclusion, we identified a novel HBV mRNA-miR-15a/16-Bcl-2 regulatory pathway that is involved in inhibiting etoposide-induced apoptosis of hepatoma cells which may contribute to facilitating HBV chronic infection and hepatoma development. |
京公网安备 11010502044263号