Brief Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jun 7, 2011; 17(21): 2674-2680
Published online Jun 7, 2011. doi: 10.3748/wjg.v17.i21.2674
Enhanced proliferation, invasion, and epithelial-mesenchymal transition of nicotine-promoted gastric cancer by periostin
Yu Liu, Bao-An Liu
Yu Liu, Bao-An Liu, Division of Basic Medicine, Department of Pathology, Central South University Xiangya School of Medicine, Changsha 410 013, Hunan Province, China
Author contributions: Liu Y and Liu BA co-designed the research; Liu Y independently performed the experiments, analyzed the data and finished the manuscript.
Supported by Department of Pathology, Division of Basic Medicine, Central South University Xiangya School of Medicine
Correspondence to: Bao-An Liu, MD, Professor, Division of Basic Medicine, Department of Pathology, Central South University Xiangya School of Medicine, #172 Tongzi Po, Yuelu District, Changsha 410013, Hunan Province, China. 1191504600@qq.com
Telephone: +86-731-82650410 Fax: +86-731-82650410
Received: December 21, 2010
Revised: April 19, 2011
Accepted: April 26, 2011
Published online: June 7, 2011
Abstract

AIM: To investigate the contribution of periostin in nicotine-promoted gastric cancer cell proliferation, survival, invasion, drug resistance, and epithelial-mesenchymal transition (EMT).

METHODS: Gastric cancer cells were treated with nicotine and periostin protein expression was determined by immunoblotting. Periostin mRNA in gastric cancer cells was silenced using small interfering RNA (siRNA) techniques and periostin gene expression was evaluated by quantitative reverse transcription-polymerase chain reaction. Gastric cancer cells transfected with control or periostin siRNA plasmid were compared in terms of cell proliferation using the methylthiazolyldiphenyl-tetrazolium bromide assay. Cell apoptosis was compared using annexin V-fluoresceine isothiocyanate and propidium iodine double staining. Tumor invasion was determined using the Boyden chamber invasion assay, and the EMT marker Snail expression was evaluated by immunoblotting.

RESULTS: Nicotine upregulated periostin in gastric cancer cells through a COX-2 dependent pathway, which was blocked by the COX-2-specific inhibitor NS398. Periostin mRNA expression was decreased by ~87.2% by siRNA in gastric cancer cells, and stable periostin-silenced cells were obtained by G418 screening. Periostin-silenced gastric cancer cells exhibited reduced cell proliferation, elevated sensitivity to chemotherapy with 5-fluorouracil, and decreased cell invasion and Snail expression (P < 0.05).

CONCLUSION: Periostin is a nicotine target gene in gastric cancer and plays a role in gastric cancer cell growth, invasion, drug resistance, and EMT facilitated by nicotine.

Keywords: Cyclooxygenase-2; Malignant growth; RNA interference; Snail; Smoking