Modulation of miR‑122 expression affects the interferon response in human hepatoma cells

Li,Aimei; Qian,Jun; He,Junming; Zhang,Qingmeng; Zhai,Aixia; Song,Wuqi; Li,Yujun; Ling,Hong; Zhong,Zhaohua; Zhang,Fengmin

doi:10.3892/mmr.2012.1233

Modulation of miR‑122 expression affects the interferon response in human hepatoma cells

Authors:
- Aimei Li
- Jun Qian
- Junming He
- Qingmeng Zhang
- Aixia Zhai
- Wuqi Song
- Yujun Li
- Hong Ling
- Zhaohua Zhong
- Fengmin Zhang
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Affiliations: Department of Microbiology, Harbin Medical University, Ministry of Education of China, Harbin 150081, P.R. China, Heilongjiang Key Laboratory of Immunity and Infection, Harbin Medical University, Ministry of Education of China, Harbin 150081, P.R. China, Bio‑pharmaceutical Key Laboratory, Harbin Medical University, Ministry of Education of China, Harbin 150081, P.R. China
Published online on: December 14, 2012 https://doi.org/10.3892/mmr.2012.1233
Pages: 585-590

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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.

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