Published online May 16, 2018. doi: 10.12998/wjcc.v6.i5.64
Peer-review started: January 15, 2018
First decision: January 22, 2018
Revised: February 9, 2018
Accepted: March 7, 2018
Article in press: March 7, 2018
Published online: May 16, 2018
Helicobacter pylori (H. pylori) is a model organism for understanding host-pathogen interactions and infection-mediated carcinogenesis. Gastric cancer and H. pylori colonization indicates the strong correlation. The progression and exacerbation of H. pylori infection are influenced by some factors of pathogen and host. Several virulence factors involved in the proper adherence and attenuation of immune defense to contribute the risk of emerging gastric cancer, therefore analysis of them is very important. H. pylori also modulates inflammatory and autophagy process to intensify its pathogenicity. From the host regard, different genetic factors particularly affect the development of gastric cancer. Indeed, epigenetic modifications, MicroRNA and long non-coding RNA received more attention. Generally, various factors related to pathogen and host that modulate gastric cancer development in response to H. pylori need more attention due to develop an efficacious therapeutic intervention. Therefore, this paper will present a brief overview of host-pathogen interaction especially emphases on bacterial virulence factors, interruption of host cellular signaling, the role of epigenetic modifications and non-coding RNAs.
Core tip: As Helicobacter pylori (H. pylori) is a model organism for understanding host-pathogen interactions and infection-mediated carcinogenesis, ongoing studies in this area should have broad relevance to these conditions. In this context, we tried to review salient host and pathogen factors that influence on gastric cancer in H. pylori infection with emphasis on bacterial virulence factors, interruption of host cellular signaling, the role of epigenetic modifications and non-coding RNAs.