PRDX2 protects against oxidative stress induced by H. pylori and promotes resistance to cisplatin in gastric cancer.
Animals
Cell Line, Tumor
Cell Proliferation
/ drug effects
Cell Survival
/ drug effects
Cisplatin
/ pharmacology
Gene Expression Regulation, Neoplastic
/ drug effects
Helicobacter Infections
/ complications
Helicobacter pylori
/ pathogenicity
Humans
Mice
Neoplasm Staging
Oxidative Stress
Peroxiredoxins
/ genetics
Prognosis
Stomach Neoplasms
/ etiology
Survival Analysis
Up-Regulation
Antioxidant response
Apoptosis
Infection
NF-κB
Oxidative DNA damage
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
29
05
2019
revised:
30
08
2019
accepted:
03
09
2019
pubmed:
20
9
2019
medline:
24
10
2020
entrez:
20
9
2019
Statut:
ppublish
Résumé
Helicobacter pylori (H. pylori) infection is the main risk factor for gastric cancer. The role of antioxidant enzyme peroxiredoxin 2 (PRDX2) in gastric tumorigenesis remains unknown. In vitro (AGS and SNU-1 cell lines) and in vivo mouse models were utilized to investigate the role of PRDX2 in response to H. pylori infection (7.13, J166 or PMSS1 strain). We detected high levels of PRDX2 expression in gastric cancer tissues. Gastric cancer patients with high expression levels of PRDX2 had significantly worse overall and progression-free survival than those with low levels. H. pylori infection induced activation of NF-κB with increased expression of PRDX2, in in vitro and in vivo models. The knockdown of PRDX2 led to an increase in the levels of reactive oxygen species (ROS), oxidative DNA damage, and double-strand DNA breaks, in response to H. pylori infection, as measured by H
Sections du résumé
BACKGROUND
Helicobacter pylori (H. pylori) infection is the main risk factor for gastric cancer. The role of antioxidant enzyme peroxiredoxin 2 (PRDX2) in gastric tumorigenesis remains unknown. In vitro (AGS and SNU-1 cell lines) and in vivo mouse models were utilized to investigate the role of PRDX2 in response to H. pylori infection (7.13, J166 or PMSS1 strain). We detected high levels of PRDX2 expression in gastric cancer tissues. Gastric cancer patients with high expression levels of PRDX2 had significantly worse overall and progression-free survival than those with low levels. H. pylori infection induced activation of NF-κB with increased expression of PRDX2, in in vitro and in vivo models. The knockdown of PRDX2 led to an increase in the levels of reactive oxygen species (ROS), oxidative DNA damage, and double-strand DNA breaks, in response to H. pylori infection, as measured by H
Identifiants
pubmed: 31536951
pii: S2213-2317(19)30551-8
doi: 10.1016/j.redox.2019.101319
pmc: PMC6811995
pii:
doi:
Substances chimiques
PRDX2 protein, human
EC 1.11.1.15
Peroxiredoxins
EC 1.11.1.15
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
101319Subventions
Organisme : NCI NIH HHS
ID : R01 CA206564
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA093999
Pays : United States
Organisme : BLRD VA
ID : I01 BX002115
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA077955
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA138833
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA240139
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA224366
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA116087
Pays : United States
Organisme : BLRD VA
ID : IK6 BX003787
Pays : United States
Organisme : BLRD VA
ID : I01 BX001179
Pays : United States
Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.
Références
Biosci Rep. 2017 May 11;37(3):
pubmed: 28432271
Gastroenterology. 2010 Dec;139(6):2005-17
pubmed: 20801119
Haematologica. 2011 Nov;96(11):1595-604
pubmed: 21750082
Gastroenterology. 2018 Nov;155(5):1372-1382.e17
pubmed: 29990487
Oxid Med Cell Longev. 2018 Apr 26;2018:1874985
pubmed: 29854076
Cancer Res. 2006 Jun 15;66(12):6080-6
pubmed: 16778180
EMBO Rep. 2009 Nov;10(11):1242-9
pubmed: 19820695
CA Cancer J Clin. 2015 Mar;65(2):87-108
pubmed: 25651787
Autophagy. 2015;11(2):239-52
pubmed: 25701194
Gastroenterology. 2013 Jan;144(1):122-133.e9
pubmed: 23058321
Neuropathol Appl Neurobiol. 2019 Aug;45(5):459-475
pubmed: 30346063
Mol Clin Oncol. 2017 Feb;6(2):139-153
pubmed: 28357082
Gut. 2015 Jul;64(7):1040-8
pubmed: 25080447
Proc Natl Acad Sci U S A. 2014 Aug 19;111(33):12157-62
pubmed: 25097261
Cell Death Dis. 2017 Jun 29;8(6):e2908
pubmed: 28661480
Oncogene. 2013 Feb 7;32(6):724-35
pubmed: 22430214
Nat Commun. 2019 Jan 18;10(1):309
pubmed: 30659176
CA Cancer J Clin. 2019 Jan;69(1):7-34
pubmed: 30620402
Int J Cancer. 2013 Sep 15;133(6):1507-12
pubmed: 23463379
Free Radic Biol Med. 2017 Mar;104:75-103
pubmed: 28062361
Redox Biol. 2015 Aug;5:319-327
pubmed: 26114584
Gastroenterology. 2016 Jan;150(1):64-78
pubmed: 26385073
Cell Rep. 2015 Oct 6;13(1):70-79
pubmed: 26411687
Neoplasia. 2018 Nov;20(11):1106-1120
pubmed: 30245403
CA Cancer J Clin. 2016 Mar-Apr;66(2):115-32
pubmed: 26808342
PLoS Pathog. 2016 Jan 13;12(1):e1005382
pubmed: 26761793
Gastroenterology. 2015 Apr;148(4):719-31.e3
pubmed: 25655557
Gut. 2017 May;66(5):761-762
pubmed: 27590997
Oncotarget. 2016 Feb 9;7(6):6379-97
pubmed: 26837221
Br J Cancer. 2011 Jan 4;104(1):110-9
pubmed: 21119665
Eur J Cancer. 2012 Nov;48(17):3186-97
pubmed: 22784549
J Transl Med. 2017 Dec 19;15(1):257
pubmed: 29258530
J Proteomics. 2015 Apr 24;119:218-29
pubmed: 25724726
Gastroenterology. 2016 May;150(5):1113-1124.e5
pubmed: 26836587
Redox Biol. 2013 Feb 01;1:115-24
pubmed: 24024144
Physiol Rev. 2016 Jan;96(1):307-64
pubmed: 26681794
Free Radic Biol Med. 2017 Apr;105:16-27
pubmed: 27682363
Cancer Lett. 2014 Feb 28;343(2):190-9
pubmed: 24125860