HERG1 functions as an oncogene in pancreatic cancer and is downregulated by miR-96
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1 Department of General Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
2 Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
3 Department of Gastroenterology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
* Contributed equally to this paper.
Dr. Zekuan Xu, e-mail: firstname.lastname@example.org
Dr. Guoxin Zhang, e-mail: email@example.com
Key words:pancreatic cancer; HERG1; miR-96; anticancer therapy
Received: April 23, 2014 Accepted: July 07, 2014 Published: July 15, 2014
Pancreatic cancer is an aggressive malignancy with an extremely poor prognosis. The human ether-a-go-go-related potassium channel (HERG1) is a human rapid delayed rectifier, which is involved in many crucial cellular events. In this article, we find that HERG1 expression is dramatically increased both in pancreatic cancer tissues and cell lines, and that increased HERG1 expression is significantly related to the development of pancreatic cancer. HERG1 silencing in pancreatic cancer-derived cell lines PANC-1 and CFPAC-1 strongly inhibits their malignant capacity in vitro as well as tumorigenicity and metastasis in nude mice. In addition, HERG1 is identified as a direct target of miR-96, which is downregulated in pancreatic cancer tissues and cell lines. Ectopic expression of miR-96 represses the HERG1 expression in pancreatic cancer and significantly inhibits malignant behavior of pancreatic cancer cells in vitro and in vivo.
Collectively, our findings suggest that miR-96 acts as a tumor suppressor in pancreatic cancer and may therefore serve as a useful therapeutic target for the development of new anticancer therapy.
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