title: HCV infection induces the upregulation of miR-221 in NF-κB dependent manner.
abstract: The upregulation of miR-221 has been reported in variety of cancer, including HCV associated HCC, the mechanism of upregulation of miR-221 however remains unclear. In this study, it was found that miR-221 was significantly upregulated in serum of patients with HCV associated chronic hepatitis (cHCV), which suggested the possible biological significance of miR-221 in HCV infection. Important, the upregulated miR-221 was positive correlation with serum miR-122, alanine aminotransferase (ALT) and aspartate transaminase (AST), which are reported as biomarkers for liver injuries. Further studies indicated that HCVcc infection activated nuclear factor-kappa B (NF-κB) and the upregulation of miR-221 by HCVcc infection could totally blocked by NF-κB inhibitor (pyrrolidine dithiocarbamate, PDTC). In conclusion, HCVcc infection could upregulate the expression of miR-221 in NF-κB dependent manner.
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
authors.forename: Cui-Ling
authors.initials: CL
authors.lastname: Ding
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
authors.forename: Gang
authors.initials: G
authors.lastname: Xu
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Ren
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
authors.forename: Lan-Juan
authors.initials: LJ
authors.lastname: Zhao
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Zhao
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China. Electronic address: qizt@smmu.edu.cn.
authors.forename: Zhong-Tian
authors.initials: ZT
authors.lastname: Qi
authors.affiliation: Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai 200433, China. Electronic address: wonwin29@126.com.
authors.forename: Wen
authors.initials: W
authors.lastname: Wang
mesh_terms: D000328:Adult; D000368:Aged; D002460:Cell Line; D005260:Female; D005786:Gene Expression Regulation; D016174:Hepacivirus; D006526:Hepatitis C / Q000235:genetics* / Q000378:metabolism* / Q000821:virology; D054884:Host-Pathogen Interactions / Q000235:genetics; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000097:blood / Q000235:genetics*; D008875:Middle Aged; D016328:NF-kappa B / Q000097:blood / Q000378:metabolism*; D015854:Up-Regulation; D055815:Young Adult
chemical_list: C549405:MIRN211 microRNA, human; D035683:MicroRNAs; D016328:NF-kappa B
keywords: HCV; NF-κB; miR-221