Analysis of the relationship between microRNA-31 and interferon regulatory factor-1 in hepatocellular carcinoma cells

被引:3
|
作者
Wan, P. -Q. [1 ,2 ]
Zhang, J. -H. [2 ,3 ]
Du, Q. [2 ]
Dong, K. [2 ,4 ]
Luo, J. [2 ,5 ]
Heres, C. [2 ]
Geller, D. A. [2 ]
机构
[1] Guangxi Med Univ, Affiliated Hosp 1, Dept Infect Dis, Nanning, Peoples R China
[2] Univ Pittsburgh, Dept Surg, Pittsburgh, PA 15260 USA
[3] Guangxi Med Univ, Affiliated Hosp 1, Dept Digest Med, Nanning, Peoples R China
[4] Guangxi Med Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Nanning, Peoples R China
[5] Xiangya Med Univ, Affiliated Hosp 2, Dept Surg, Changsha, Peoples R China
关键词
GMIR-31; IRF-1; Hepatocellular carcinoma; Relationship; GROWTH-INHIBITION; TUMOR-SUPPRESSOR; POOR-PROGNOSIS; CANCER; EXPRESSION; MIR-31; TARGET;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: MicroRNAs (miRNAs) play a role in the pathogenesis of hepatocellular carcinoma (HCC). This study was designed to elucidate the role of microRNA-31 (miR-31) in HCC. MATERIALS AND METHODS: HuH7 cell lines were transfected with miR-31 mimic or miR-31 inhibitor to investigate the role of miR-31 in regulating interferon regulatory factor-1 (IRF-1). The mRNA and protein expression levels of IRF-1 were quantitatively detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. Subsequently, Dual-Luciferase reporter assay was also performed. RESULTS: The expression level of miR-31 was significantly up-regulated in HuH7 cells when compared with that in primary human hepato-cytes (hHC). Dual-Luciferase reporter assay indicated that IRF-1 was the direct target of miR-31. The expression levels of IRF-1 were decreased in HuH7 and HepG2 cell lines. IRF-1 was negatively correlated with miR-31 in HCC tissues and paired adjacent tissues. The expression level of miR-31 was inversely correlated with IRF-1. MiR-31 inhibitor up-regulated the expression levels of IRF-1 in HuH7 cells, whereas miR-31 mimic down-regulated the expression levels of IRF-1. Furthermore, the miR-31 mimic repressed IRF-1-3'UTR reporter activity, whereas the miR-31 inhibitor enhanced IRF-1-3'UTR reporter activity depending on the concentration of miR-31 mimic and miR-31 inhibitor. CONCLUSIONS: These results indicated that miR-31 can regulate the expression level of IRF-1 in HCC, which probably provided novel theoretical evidence for the application of target miR-31 treatment of HCC.
引用
收藏
页码:647 / 654
页数:8
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