MiR-494-3p promotes PI3K/AKT pathway hyperactivation and human hepatocellular carcinoma progression by targeting PTEN

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作者
Hui Lin
Zhi-Ping Huang
Jiao Liu
Yun Qiu
Yuan-ping Tao
Meng-chao Wang
Hui Yao
Ke-zhu Hou
Fang-ming Gu
Xuan-fu Xu
机构
[1] Shidong Hospital,The First Department of General Surgeny
[2] Yangpu District,Department of Radiotherapy, Shidong Hospital
[3] Shanghai,Department of Gastroenterology, Shidong Hospital
[4] Anhui Medical University,The Third Department of Hepatic Surgery
[5] Yangpu District,Department of Hepatobiliary Surgery
[6] Shanghai,undefined
[7] Anhui Medical University,undefined
[8] Yangpu District,undefined
[9] Shanghai,undefined
[10] Anhui Medical University,undefined
[11] Eastern Hepatobiliary Surgery Hospital,undefined
[12] Second Military Medical University,undefined
[13] Shanghai Public Health Clinical Center Affiliated to Fudan University,undefined
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摘要
Recent studies have shown that miR-494-3p is oncogene and has a central role in many solid tumors; however, the role of miR-494-3p in the progression and prognosis of hepatocellular carcinoma (HCC) remains unknown. In this study, it was found that miR-494-3p was up-regulated in HCC tissues. The high level of miR-494-3p in HCC tumors was correlated with aggressive clinicopathological characteristics and predicted poor prognosis in HCC patients. Functional study demonstrated that miR-494-3p significantly promoted HCC cell metastasis in vitro and vivo. Since phosphoinositide 3-kinase/protein kinase-B (PI3K/AKT) signaling is a basic oncogenic driver in HCC, a potential role of miR-494-3p was explored as well as its target genes in PI3K/AKT activation. Of all the predicted target genes of miR-494-3p, the tumor-suppressor phosphatase and tensin homolog (PTEN) were identified. In conclusion, the data we collected could define an original mechanism of PI3K/AKT hyperactivation and sketch the regulatory role of miR-494-3p in suppressing the expression of PTEN. Therefore, targeting miR-494-3p could provide an effective therapeutic method for the treatment of the disease.
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