Oncotarget

Research Papers:

miR-211 suppresses hepatocellular carcinoma by downregulating SATB2

Guixing Jiang, Yunfu Cui, Xin Yu, Zhengrong Wu, Guoping Ding _ and Liping Cao

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Oncotarget. 2015; 6:9457-9466. https://doi.org/10.18632/oncotarget.3265

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Abstract

Guixing Jiang1, Yunfu Cui2, Xin Yu3, Zhengrong Wu1, Guoping Ding1, Liping Cao1

1Department of Hepatopancreatobiliary Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China

2Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China

3Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing, China

Correspondence to:

Liping Cao, e-mail: caolipingzju@126.com

Keywords: hepatocellular carcinoma, microRNAs, miR-211, SATB2

Received: January 08, 2015     Accepted: January 31, 2015     Published: March 25, 2015

ABSTRACT

Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC.


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