Molecular Signaling in Tumorigenesis of Gastric Cancer

Iran Biomed J. 2018 Jul;22(4):217-30. doi: 10.22034/ibj.22.4.217. Epub 2018 Apr 30.

Abstract

Gastric cancer (GC) is regarded as the fifth most common cancer and the third cause of cancer-related deaths worldwide. Mechanism of GC pathogenesis is still unclear and relies on multiple factors, including environmental and genetic characteristics. One of the most important environmental factors of GC occurrence is infection with Helicobacter pylori that is classified as class one carcinogens. Dysregulation of several genes and pathways play an essential role during gastric carcinogenesis. Dysregulation of developmental pathways such as Wnt/β-catenin signaling, Hedgehog signaling, Hippo pathway, Notch signaling, nuclear factor-kB, and epidermal growth factor receptor have been found in GC. Epithelial-mesenchymal transition, as an important process during embryogenesis and tumorigenesis, is supposed to play a role in initiation, invasion, metastasis, and progression of GC. Although surgery is the main therapeutic modality of the disease, the understanding of biological processes of cell signaling pathways may help to develop new therapeutic targets for GC.

Keywords: Beta Catenin; Epithelial-mesenchymal transition; Hedgehogs; Helicobacter pylori; NF-kappa B.

Publication types

  • Review

MeSH terms

  • Carcinogenesis
  • Cell Transformation, Neoplastic*
  • Epithelial-Mesenchymal Transition
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • Gene Expression Regulation, Neoplastic*
  • Genetic Markers
  • Genetic Predisposition to Disease
  • Helicobacter Infections / metabolism
  • Helicobacter Infections / pathology*
  • Helicobacter pylori*
  • Humans
  • Matrix Metalloproteinases / metabolism
  • Neoplasm Invasiveness
  • Receptor, ErbB-2 / genetics
  • Receptor, ErbB-2 / metabolism
  • Risk Factors
  • Signal Transduction
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / metabolism*
  • Stomach Neoplasms / microbiology
  • Wnt Proteins / metabolism
  • Wnt Signaling Pathway
  • beta Catenin / metabolism

Substances

  • Genetic Markers
  • Wnt Proteins
  • beta Catenin
  • EGFR protein, human
  • ERBB2 protein, human
  • ErbB Receptors
  • Receptor, ErbB-2
  • Matrix Metalloproteinases