Basic Study
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 28, 2018; 24(40): 4565-4577
Published online Oct 28, 2018. doi: 10.3748/wjg.v24.i40.4565
Helicobacter pylori promotes invasion and metastasis of gastric cancer by enhancing heparanase expression
Li-Ping Liu, Xi-Ping Sheng, Tian-Kui Shuai, Yong-Xun Zhao, Bin Li, Yu-Min Li
Li-Ping Liu, The Second Clinical Medical School of Lanzhou University, Lanzhou 730000, Gansu Province, China
Li-Ping Liu, Bin Li, Department of Critical Care Medicine, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu Province, China
Li-Ping Liu, Tian-Kui Shuai, Department of Critical Care Medicine, The Donggang District of First Hospital of Lanzhou University, Lanzhou 730030, Gansu Province, China
Xi-Ping Sheng, Institute of Epidemiology and Health Statistics, School of Public Health, Lanzhou University, Lanzhou 730000, Gansu Province, China
Yong-Xun Zhao, Department of Surgical Oncology, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu Province, China
Yu-Min Li, Key Laboratory of Digestive System Tumors of Gansu Province, The Second Clinical Medical School of Lanzhou University, Lanzhou 730000, Gansu Province, China
Author contributions: Liu LP and Li YM designed the experiments; Sheng XP and Li B contributed to the statistical analyses; Zhao YX performed the experiments; Liu LP prepared the manuscript; Shuai TK and Li B conducted data collection.
Supported by the Natural Science Foundation of Gansu Province, No. 1506RJZA255; the National Natural Science Foundation of China, No. 81572437; the Open Topics of the Key Laboratory of Biological Treatment and Regenerative Medicine in Gansu Province, No. zdsyskfkt-201702; and the Fund of Donggang Branch, The First Hospital of Lanzhou University, No. ldyydgyn-201705.
Institutional review board statement: The study was approved by the Ethics Review Board of the First Hospital of Lanzhou University.
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: No additional unpublished data are available.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: Yu-Min Li, MD, PhD, Chief Doctor, Professor, Key Laboratory of Digestive System Tumors of Gansu Province, The Second Clinical Medical School of Lanzhou University, No. 82, Cuiyingmen, Chengguan District, Lanzhou 730000, Gansu Province, China. liym@lzu.edu.cn
Telephone: +86-931-8912127 Fax: +86-931-8912127
Received: August 11, 2018
Peer-review started: August 13, 2018
First decision: August 27, 2018
Revised: September 2, 2018
Accepted: October 5, 2018
Article in press: October 5, 2018
Published online: October 28, 2018
Processing time: 76 Days and 21.5 Hours
ARTICLE HIGHLIGHTS
Research background

The underlying mechanism that Helicobacter pylori (H. pylori) infection results in gastric cancer (GC) is still unknown. Heparanase (HPA) leads to the invasion and metastasis of GC. However, it is not clear whether H. pylori infection in GC increases HPA expression. Such finding suggests that HPA may become a therapeutic target for GC with H. pylori infection.

Research motivation

Although there have been increasing numbers of studies indicating that H. pylori infection results in GC, the underlying mechanism is still unknown. HPA is expressed in many tumours and leads to the invasion and metastasis of tumour, especially in GC. H. pylori infection can induce the development of GC by activating mitogen-activated protein kinase (MAPK) which is closely related to the expression of HPA. However, it is not clear whether MAPK is involved in the regulation of HPA expression following H. pylori infection that leads to GC.

Research objectives

To detect the mechanisms of H. pylori infection in the invasion and metastasis of GC.

Research methods

Immunohistochemistry method was used to detect H. pylori infection and HPA and MAPK expression in GC tissue, and their association with the clinical features of GC was analysed with SPSS 22.0. Kaplan-Meier method and COX proportional models were used to analyse prognosis. HPA and MAPK expression in MKN-45 cells infected with H. pylori was analysed using Western blot.

Research results

This study demonstrates that H. pylori infection increases HPA expression in GC, which is likely mediated via activation of the MAPK signaling pathway.

Research conclusions

The current study shows that H. pylori infection is involved in the invasion and metastasis of GC by upregulating HPA expression, which is likely mediated via activation of the MAPK signaling pathway. HPA is an important factor for predicting the prognosis and relapse of GC with H. pylori infection.

Research perspectives

HPA may become a therapeutic target for GC with H. pylori infection.