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摘要：
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摘要：目的 探讨microRNA-520a（miR-520a）抑制HepG2.2.15细胞中HBV DNA复制的机制。方
法 通过Entrez Nucleotide数据库预测AKT是否为miRNA-520a的靶基因。通过RT-qPCR和Western blot
验证miRNA-520a是否调控HepG2.2.15细胞中AKT的表达，研究miRNA-520a模拟物及其抑制剂对
HepG2.2.15细胞中HBV DNA转录和复制的影响。评价siRNA对AKT mRNA和蛋白表达以及HBV DNA
转录和复制的作用。结果 在HepG2.2.15细胞中，AKT为miRNA-520a的靶基因，miRNA-520a通过抑
制AKT表达可进一步抑制HepG2.2.15细胞中HBV DNA的转录和复制。AKT表达下调受siRNAs诱导，
同时抑制HepG2.2.15细胞中HBV的转录和复制。结论 MiRNA-520a可抑制AKT表达，进而抑制HBV
DNA转录和复制，其可能成为治疗HBV感染的新靶点。
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Abstract: Objective To investigate the mechanism of replication inhibition of HBV DNA in HepG2.2.15 cells
through inactivated AKT regulated by miR-520a. Methods The online Entrez Nucleotide database was taken
to identify whether AKT was the target gene of miRNA-520a. RT-qPCR and Western blot assay were applied
to confirm whether miRNA-520a regulate the expression of AKT in HepG2.2.15 cells. Moreover, the effects of
miRNA-520a on transcription and replication of HBV DNA in HepG2.2.15 was assessed. The roles of siRNA
on the expression of AKT mRNA and protein, also HBV transcription and replication were evaluated. Results In
HepG2.2.15 cells, AKT was the target gene of miRNA-520a, miRNA-520a could control the transcription and
replication of HBV DNA by inhibiting AKT expression. AKT expression was down-regulated significantly by its
siRNAs, which gave rise to a remarkable suppression of HBV transcription and replication in HepG2.2.15 cells.
Conclusions MiRNA-520a led to the inhibition of AKT expression, and then inhibited the transcription and
replication of HBV DNA. It was shown that miRNA-520a may be a novel target for treatment of HBV infection.
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