Activation of EGFR and ERBB2 by Helicobacter pylori results in survival of gastric epithelial cells with DNA damage.
AUTHORS
Chaturvedi
RRupesh ,
Asim
M Mohammad ,
Piazuelo
MB M Blanca ,
Yan
F Fang ,
Barry
DP Daniel P ,
Sierra
JC Johanna Carolina ,
Delgado
AG Alberto G ,
Hill
S Salisha ,
Casero
RA Robert A ,
Bravo
LE Luis E ,
Dominguez
RL Ricardo L ,
Correa
P Pelayo ,
Polk
DB D Brent ,
Washington
MK M Kay ,
Rose
KL Kristie L ,
Schey
KL Kevin L ,
Morgan
DR Douglas R ,
Peek
RM Richard M ,
Wilson
KT Keith T .
Gastroenterology. 2014 6 ; 146(7).
1739-51.e14
- PMCID: PMC4035375.
- NIHMSID: NIHMS568372
ABSTRACT
The gastric cancer-causing pathogen Helicobacter pylori up-regulates spermine oxidase (SMOX) in gastric epithelial cells, causing oxidative stress-induced apoptosis and DNA damage. A subpopulation of SMOX(high) cells are resistant to apoptosis, despite their high levels of DNA damage. Because epidermal growth factor receptor (EGFR) activation can regulate apoptosis, we determined its role in SMOX-mediated effects.