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目的探讨mi R-122在乙肝病毒复制和乙肝相关性肝癌发病机制中的作用。方法构建mi R-122表达载体并转染Hep G2.2.15细胞,预测mi R-122作用靶点,Western blot检测转染细胞Gyclin G1蛋白表达,QPCR检测转染细胞和肝癌组织中mi R-122的表达,HBV-DNA定量检测转染组细胞HBV表达,MTT法检测mi R-122对细胞增殖的影响,Annexinⅴ/PI荧光双染技术分析mi R-122诱导的细胞凋亡情况。肝癌组织和配对癌旁组织样本各来自3例乙肝相关性肝癌病人。结果与配对的癌旁组织比较,肝癌组织中mi R-122表达低下。mi R-122转染Hep G2.2.15后表达显著上调而Cyclin G1表达下调,mi R-122转染细胞后明显抑制HBV的复制,并诱导细胞凋亡和抑制增殖(P<0.01)。结论 mi R-122可下调靶基因Cyclin G1的表达,上调mi R-122可以抑制HBV基因的复制并促进HBV相关性肝癌的发生发展。
Objective To explore the role of mi R-122 in the pathogenesis of hepatitis B virus replication and hepatitis B-related liver cancer. Methods The mi R-122 expression vector was constructed and transfected into Hep G2.2.15 cells to predict the target of mi R-122. The expression of Gyclin G1 protein was detected by Western blot. The expression of mi R-122 was detected by QPCR in transfected cells and hepatocellular carcinoma The expression of HBV in transfected cells was detected by HBV-DNA. The effect of mi R-122 on cell proliferation was detected by MTT assay. The apoptosis induced by mi R-122 was analyzed by Annexin ⅴ / PI double staining. Liver cancer tissues and paired paracancerous tissue samples from each of three cases of hepatitis B-related liver cancer patients. Results Compared with matched paracancerous tissues, the expression of mi R-122 in HCC tissues was low. The expression of Cyclin G1 was significantly up-regulated after mi R-122 transfected Hep G2.2.15, and was inhibited by mi R-122 after transfected with mi R-122. The mi R-122 also induced apoptosis and inhibited the proliferation of cells (P <0.01). Conclusion mi R-122 can down-regulate the expression of target gene Cyclin G1. Up-regulation of mi R-122 can inhibit the replication of HBV gene and promote the development of HBV-related hepatocellular carcinoma.