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.
Highlights
Hepatocellular carcinoma (HCC) is the sixth most prevalent cancer and the third most frequent cause of cancer mortality worldwide, leading to more than 600,000 deaths each year [1, 2]
Our study showed that miR-211 expression was downregulated in HCC cells and HCC tissues
As for the mechanism, our results indicated that miR-211 directly targeted SATB2 to inhibit cell proliferation and invasion in HCC cells
Summary
Hepatocellular carcinoma (HCC) is the sixth most prevalent cancer and the third most frequent cause of cancer mortality worldwide, leading to more than 600,000 deaths each year [1, 2]. HCC is especially common in China, with the mortality rate the second highest [3]. In China, more than 110 000 people die from liver cancer each year, causing 45% of the liver cancer death in the world [3]. The 5-year survival rate of HCC is still below 5% [4,5,6]. It is urgent to develop novel strategies for the early diagnosis, prediction of the prognosis and therapeutic target of patients with HCC
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