Cells (Apr 2020)

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in <i>Helicobacter pylori</i>-Induced Gastric Cancer

  • Jacek Baj,
  • Izabela Korona-Głowniak,
  • Alicja Forma,
  • Amr Maani,
  • Elżbieta Sitarz,
  • Mansur Rahnama-Hezavah,
  • Elżbieta Radzikowska,
  • Piero Portincasa

DOI
https://doi.org/10.3390/cells9041055
Journal volume & issue
Vol. 9, no. 4
p. 1055

Abstract

Read online

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

Keywords