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Published on: June 5, 2020
The IL-6/STAT3 pathway upregulates microRNA-125b expression in hepatitis C virus infection
Chia-Yen Dai1,2,3,4,5,6, Yi-Shan Tsai1, Wen-Wen Chou1
1Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Background/Aims:
MicroRNA-125b (miR-125b) has been found to regulate inflammation and acts as an oncogene in many cancers. The mechanisms of miR-125b expression during hepatitis C virus (HCV) infection remain to be clarified. The present study aims to identify the factors that might regulate miR-125b expression in HCV infection.
Results:
High expression of miR-125b was found to correlate with HCV infection in replicon cells and in sera from HCV-infected patients, whereas the miR-125b inhibitor reduced HCV gene expression. The interleukin 6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) pathway plays an inducible effect on miR-125b gene expression. STAT3 siRNA or inhibitor could reduce HCV replication.
Materials And Methods:
HCV replicon cells Con1 (type 1b) and Huh7/Ava5 (type 1b) were treated with 17-hydroxy-jolkinolide B (HJB) or STAT3 siRNA. Cell viability assay and Renilla Luciferase Assay were used. Fragments of the miR-125b-1 promoter were constructed for the luciferase reporter assay. PSMB8, PSMB9, miR-125b-1, and miR-125b-2 expression was determined using TaqMan® Gene Expression Assays. Western blot analysis was performed to assess protein abundance.
Conclusions:
This study elucidates a novel pathway for miR-125b in the pathogenesis of chronic HCV infection and suggests it as a possible target for treating HCV infection.
Insights
MicroRNA-125b (miR-125b) expression is elevated in hepatitis C virus (HCV) infection. Targeting the IL-6/STAT3 pathway and miR-125b may offer new treatments for HCV.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- MicroRNA-125b (miR-125b) is implicated in inflammation and cancer.
- The role of miR-125b in hepatitis C virus (HCV) infection is not fully understood.
Purpose of the Study:
- To investigate the regulatory mechanisms of miR-125b expression during HCV infection.
- To identify potential therapeutic targets for HCV.
Main Methods:
- HCV replicon cells were treated with 17-hydroxy-jolkinolide B or STAT3 siRNA.
- Luciferase reporter assays and TaqMan Gene Expression Assays were employed.
- Western blot analysis assessed protein levels.
Main Results:
- miR-125b expression correlated with HCV infection in cells and patient sera.
- Inhibiting miR-125b reduced HCV gene expression.
- The IL-6/STAT3 pathway induced miR-125b expression, and STAT3 inhibition decreased HCV replication.
Conclusions:
- A novel pathway involving miR-125b in HCV pathogenesis was identified.
- miR-125b presents a potential therapeutic target for HCV infection.
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