Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2018 (2018), Article ID 3195025, 10 pages
https://doi.org/10.1155/2018/3195025
Research Article

Suppression of IL-6 Gene by shRNA Augments Gemcitabine Chemosensitization in Pancreatic Adenocarcinoma Cells

1Department of ICU, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China
2Department of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China
3Department of Medical Oncology, The Affiliated Hospital of Hangzhou Normal University, Zhejiang University, Hangzhou, China

Correspondence should be addressed to Da Li; nc.ude.ujz@wenocnoadil

Received 16 October 2017; Revised 19 January 2018; Accepted 29 January 2018; Published 6 March 2018

Academic Editor: Tao Huang

Copyright © 2018 Hai-Bo Xing et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Pancreatic adenocarcinoma has an exceedingly poor prognosis, accounting for five-year survival of less than 5%. Presently, improving the efficacy of pancreatic adenocarcinoma treatment has been the focus of medical researchers worldwide. Recently, it has been suggested that deregulation of interleukin- (IL-) 6 is caused by a key gene involved in the beginning and development of pancreatic adenocarcinoma. Herein, we investigated whether suppression of IL-6 could augment gemcitabine sensitivity in the PANC-1 cells. We found considerably higher expression of IL-6 in pancreatic adenocarcinoma tissues than that in the adjacent nontumorous tissues. Suppression of IL-6 by shRNA resulted in apoptosis as well as inhibition of cell proliferation and tumorigenicity. In addition, suppression of IL-6 remarkably promoted antitumor effect of gemcitabine, indicating that the combination of shRNA targeting IL-6 with gemcitabine may provide a potential clinical approach for pancreatic cancer therapy.