Oncotarget

Research Papers:

MiR-590-3p suppresses epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma by inhibiting SIP1 expression

Chao Zu, Shizhang Liu, Wei Cao, Zongzhi Liu, Hui Qiang, Yong Li, Chong Cheng, Le Ji, Jianhui Li and Jingyuan Li _

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Oncotarget. 2017; 8:34698-34708. https://doi.org/10.18632/oncotarget.16150

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Abstract

Chao Zu1, Shizhang Liu2, Wei Cao1, Zongzhi Liu2, Hui Qiang2, Yong Li2, Chong Cheng1, Le Ji2, Jianhui Li1 and Jingyuan Li2

1Department of Surgical Oncology, Shaanxi Provincial People’s Hospital, The Third Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710068, Shaanxi Province, P.R. China

2Department of Orthopaedics, Shaanxi Provincial People’s Hospital, The Third Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710068, Shaanxi Province, P.R. China

Correspondence to:

Jingyuan Li, email: jingyuanli@outlook.com

Keywords: intrahepatic cholangiocarcinoma, miR-590-3p, SIP1, metastasis, EMT

Received: December 20, 2016     Accepted: February 08, 2017     Published: March 13, 2017

ABSTRACT

The functional roles and clinical significances of miR-590-3p in ICC remain unclear. In the current study, we investigated the expression of miR-590-3p in tissues and sera of ICC by real-time quantitative polymerase chain reaction. We found miR-590-3p was significantly down-regulated in the sera and tissues of ICC patients, especially in those patients with lymph node metastasis or distant metastasis. AUC curves and Cox proportional hazards mode revealed serum miR-590-3p could be novel diagnostic and prognostic biomarker for ICC patients. MiR-590-3p dramatically suppressed epithelial-mesenchymal transition, cell migration, and invasion of ICC cells. SIP1 was identified as direct and functional target of miR-590-3p in ICC cells by luciferase assays. Finally, we found SIP1 expression was inversely correlated with miR-590-3p and closely related to diminished survival in ICC patients. These findings reveal functional and mechanistic roles of miR-590-3p and EMT activator SIP1 in the pathogenesis of ICC.


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