MiRNA-22 inhibits oncogene galectin-1 in hepatocellular carcinoma
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Yu You1, Jia-Xin Tan1, Hai-Su Dai1, Hao-Wei Chen1, Xue-Jun Xu1, Ai-Gang Yang1, Yu-Jun Zhang1, Lian-Hua Bai1, Ping Bie1
1Department of Hepatobiliary Surgery Institute, South Western Hospital, Third Military Medical University, Chongqing 400038, China
Ping Bie, email: [email protected]
Lian-Hua Bai, email: [email protected]
Keywords: hepatocellular carcinoma, hepatic stellate cells, galectin-1, miRNA-22
Received: April 14, 2016 Accepted: July 10, 2016 Published: August 1, 2016
Hepatic stellate cells (HSCs) induce immune privilege and promote hepatocellular carcinoma (HCC) by suppressing the immune system. On the other hand, galectin-1 and miRNA-22 (miR-22) are dysregulated in HCC and serve as prognostic indicators for patients. In this study, therefore, we measured galectin-1 and miR-22 expression in HSCs isolated from HCC tissues (Ca-HSCs), and in normal liver tissues (N-HSCs) as a control. We also investigated the apoptosis rate among T cells and the production of cytokines (IFN-γ and IL-10) in HSCs co-cultured with T cells. And we used immunohistochemical staining to tested for correlation between galectin-1 expression, CD3 expression and clinicopathological features in 162 HCC patients. Our results showed that galectin-1 expression was much higher in Ca-HSCs than in N-HSCs. Overexpression of galectin-1 promoted HSC-induced T cell apoptosis and cytokine production (IFN-γ and IL-10), while miR-22 expression inhibited it. Galectin-1 expression correlated negatively with miR-22 expression in HSCs. High galectin-1 and low CD3 expression levels were associated with poor prognosis in HCC patients. These results suggest that the immunosuppressive microenvironment promoted by HSC-derived galectin-1 in HCC can be inhibited by miR-22. Galectin-1 and miR-22 could potentially serve as prognostic markers and therapeutic targets in HCC.
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