Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 7, 2017; 23(9): 1594-1601
Published online Mar 7, 2017. doi: 10.3748/wjg.v23.i9.1594
miR-1181 inhibits invasion and proliferation via STAT3 in pancreatic cancer
Jie Wang, Xing-Jun Guo, You-Ming Ding, Jian-Xin Jiang
Jie Wang, Department of Hepatic-Biliary-Pancreatic Surgery, The Affiliated Hospital of Guizhou Medical University, Guiyang 550000, Guizhou Province, China
Xing-Jun Guo, Department of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
You-Ming Ding, Jian-Xin Jiang, Department of Hepatic-Biliary-Pancreatic Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
Author contributions: Wang J and Guo XJ contributed equally to this work; Wang J performed the majority of experiments and analyzed the data; Guo XJ performed the molecular investigations; Guo XJ, Ding YM and Jiang JX designed and coordinated the research; Wang J, Guo XJ and Jiang JX wrote the paper.
Supported by The National Natural Science Foundation of China, No. 81160311 and No. 81572429 to Jiang JX.
Institutional review board statement: The project was reviewed by the local Research and audit Department and approved without the need for the further ethical approval.
Conflict-of-interest statement: No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.
Data sharing statement: No additional data are available
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Jian-Xin Jiang, Department of Hepatic-Biliary-Pancreatic Surgery, Renmin Hospital of Wuhan University, 99 Ziyang Road, Wuhan 430030, Hubei Province, China. jjx731003@163.com
Telephone: +86-27-88041911 Fax: +86-27-88041911
Received: July 7, 2016
Peer-review started: July 13, 2016
First decision: September 28, 2016
Revised: October 9, 2016
Accepted: February 7, 2017
Article in press: February 8, 2017
Published online: March 7, 2017
Abstract
AIM

To examine the role of microRNA 1181 (miR-1181) in invasion and proliferation in pancreatic cancer.

METHODS

We analyzed the expression of miR-1181 in several pancreatic cancer cell lines and generated stable MIA-PaCa-2 and PANC-1 cell lines with up-regulated miR-1181 expression using an adenovirus delivery system. We then investigated miR-1181's effect on invasion and proliferation of pancreatic cancer cells by transwell assay, wound healing assay, cell counting kit-8 assay and colony-forming assay, and explored any underlying mechanisms by western bolt. Beyond that, we observed the change of the PANC-1 cell's cytoskeleton by immunofluorescence staining.

RESULTS

Our data showed that miR-1181 was relatively down-regulated in pancreatic cancer cell lines compared with normal pancreatic ductal epithelial cells. And miR-1181 inhibited the migration, invasion and proliferation activities of MIA-PaCa-2 and PANC-1 cells. Notably, after over-expressing of miR-1181 in PANC-1 cells, F-actin depolymerized. Immunofluorescence staining shows decreased F-actin and β-tubulin expression in PANC-1 cells over-expressing miR-1181 compared with the control cells. Furthermore, we found that over-expressing miR-1181 inhibited the expression of signal transducer and activator of transcription 3 (STAT3) while knocking-down miR-1181 up-regulated the expression of STAT3. Knocking-down miR-1181 promoted the invasion and proliferation of pancreatic cancer cells. And inhibition of STAT3 blocked the promotion effects of knocking-down miR-1181 on proliferation and invasion in pancreatic cancer.

CONCLUSION

Together our findings suggest that miR-1181 may be involved in pancreatic cancer cell invasion and proliferation by targeting STAT3 and indicate that miR-1181 may be a potential therapeutic agent for pancreatic cancer.

Keywords: Pancreatic cancer, miR-1181, Proliferation, Invasion, STAT3

Core tip: We found that miR-1181 may be involved in pancreatic cancer cell invasion and proliferation by targeting signal transducer and activator of transcription 3. Our findings suggest that miR-1181 may be a potential therapeutic agent for pancreatic cancer.