title: Modulation of miR‑122 expression affects the interferon response in             human hepatoma cells.
abstract: Type I interferon (IFN) is believed to play significant roles in limiting tumor growth. It has been revealed that the induction of endogenous IFN expression is one of the key mechanisms for successful IFN therapy. However, recent studies have shown that the efficacy of type I IFN therapy has limitations in the clinical treatment of certain tumors, including hepatocellular carcinoma (HCC). It has been revealed that the expression of miR‑122 is significantly decreased in HCC and that restoration of miR‑122 expression may improve the prognosis of this condition. Previous studies also showed that patients with low miR‑122 levels in the liver responded poorly to the IFN therapy. We previously identified that the IFN expression was reduced when miR‑122 was suppressed in human oligodendrocytes. Based on these studies, it was hypothesized that the expression of miR‑122 may modulate the endogenous IFN expression and subsequently affect the treatment outcome of IFN therapy for HCC. The results of the present study showed that miR‑122‑abundant Huh7 cells responded more significantly than miR‑122‑deficient HepG2 cells when treated with exogenous IFN. Upregulation of miR‑122 significantly increased the ability of exogenous IFN‑induced IFN expression, while downregulation of miR‑122 decreased this ability. These data indicate that a high level of miR‑122 expression may promote the expression of type I IFN induced by exogenous IFNs and further contribute to IFN therapy for HCC.
authors.affiliation: Department of Microbiology, Harbin Medical University, Ministry                     of Education of China, Harbin 150081, P.R. China.
authors.forename: Aimei
authors.initials: A
authors.lastname: Li
authors.forename: Jun
authors.initials: J
authors.lastname: Qian
authors.forename: Junming
authors.initials: J
authors.lastname: He
authors.forename: Qingmeng
authors.initials: Q
authors.lastname: Zhang
authors.forename: Aixia
authors.initials: A
authors.lastname: Zhai
authors.forename: Wuqi
authors.initials: W
authors.lastname: Song
authors.forename: Yujun
authors.initials: Y
authors.lastname: Li
authors.forename: Hong
authors.initials: H
authors.lastname: Ling
authors.forename: Zhaohua
authors.initials: Z
authors.lastname: Zhong
authors.forename: Fengmin
authors.initials: F
authors.lastname: Zhang
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D056945:Hep G2 Cells; D006801:Humans; D007370:Interferon Type I / Q000378:metabolism*; D016898:Interferon-alpha / Q000235:genetics / Q000494:pharmacology / Q000627:therapeutic use; D016899:Interferon-beta / Q000235:genetics / Q000494:pharmacology / Q000627:therapeutic use; D008113:Liver Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009836:Oligodendroglia / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D007370:Interferon Type I; D016898:Interferon-alpha; C531907:MIRN122 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D011994:Recombinant Proteins; D016899:Interferon-beta