RUNX3 regulates hepatocellular carcinoma cell metastasis via targeting miR-186/E-cadherin/EMT pathway
Metrics: PDF 564 views | HTML 1400 views | ?
Yuli Gou1,*, Fangbing Zhai2,*, Liang Zhang3 and Lan Cui4
1Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
2Department of Radiology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
3Department of Interventional Therapy, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
4Department of Ophthalmology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
*These authors have contributed equally to this work as the co-first authors
Liang Zhang, email: email@example.com
Lan Cui, email: firstname.lastname@example.org
Keywords: RUNX3, miR-186, E-cadherin, HCC
Received: May 04, 2017 Accepted: May 23, 2017 Published: June 09, 2017
Runt-related transcription factor 3 (RUNX3) has been reported as a tumor suppressor in some kinds of cancers. In the present study, hepatocellular carcinoma (HCC) microarray analysis showed that RUNX3 expression was significantly lower in HCC tissues compared with that in adjacent non-tumor tissues, and was negatively associated with metastasis and TNM stage. RUNX3 was an independently prognostic factor for 5-year overall and disease-free patient survival. Mechanically, RUNX3 repressed metastasis and invasion of HCC, and increased E-cadherin expression. RUNX3 also repressed microRNA-186 to increase E-cadherin expression. We demonstrated that miR-186 mimics attenuated RUNX3-induced increase of E-cadherin and inhibition of metastasis and invasion. In conclusion, RUNX3 suppressed HCC cell migration and invasion by targeting the miR-186/E-cadherin/EMT pathway. RUNX3 may be recommended as an effective prognostic indicator and therapeutic target for patients with HCC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.