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MSRC Mass Spectrometry Research and Development

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

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.

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.