Helicobacter pylori-induced miR-135b-5p promotes cisplatin resistance in gastric cancer.
Animals
Antineoplastic Agents
/ pharmacology
Apoptosis
Cell Proliferation
Cisplatin
/ pharmacology
Drug Resistance, Neoplasm
Gastric Mucosa
/ drug effects
Gene Expression Regulation, Neoplastic
Helicobacter Infections
/ complications
Helicobacter pylori
/ isolation & purification
Humans
Kruppel-Like Factor 4
Kruppel-Like Transcription Factors
/ genetics
Mice
Mice, Knockout
MicroRNAs
/ genetics
NF-kappa B
/ genetics
Prognosis
Stomach Neoplasms
/ drug therapy
Survival Rate
Trefoil Factor-1
/ physiology
Tumor Cells, Cultured
None
KLF4
inflammation
microRNA
tff1 knockout
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
pubmed:
10
7
2018
medline:
10
7
2019
entrez:
10
7
2018
Statut:
ppublish
Résumé
Helicobacter pylori infection is a major risk factor for the development of gastric cancer. Aberrant expression of microRNAs is strongly implicated in gastric tumorigenesis; however, their contribution in response to H. pylori infection has not been fully elucidated. In this study, we evaluated the expression of miR-135b-5p and its role in gastric cancer. We describe the overexpression of miR-135b-5p in human gastric cancer tissue samples compared with normal tissue samples. Furthermore, we found that miR-135b-5p is also up-regulated in gastric tumors from the trefoil factor 1-knockout mouse model. Infection with H. pylori induced the expression of miR-135b-5p in the in vitro and in vivo models. miR-135b-5p induction was mediated by NF-κB. Treatment of gastric cancer cells with TNF-α induced miR-135b-5p in a NF-κB-dependent manner. Mechanistically, we found that miR-135b-5p targets Krüppel-like factor 4 (KLF4) and binds to its 3' UTR, leading to reduced KLF4 expression. Functionally, high levels of miR-135b-5p suppress apoptosis and induce cisplatin resistance. Our results uncovered a mechanistic link between H. pylori infection and miR-135b-5p-KLF4, suggesting that targeting miR-135b-5p could be a potential therapeutic approach to circumvent resistance to cisplatin.-Shao, L., Chen, Z., Soutto, M., Zhu, S., Lu, H., Romero-Gallo, J., Peek, R., Zhang, S., El-Rifai, W. Helicobacter pylori-induced miR-135b-5p promotes cisplatin resistance in gastric cancer.
Identifiants
pubmed: 29985646
doi: 10.1096/fj.201701456RR
pmc: PMC6355059
doi:
Substances chimiques
Antineoplastic Agents
0
KLF4 protein, human
0
Klf4 protein, mouse
0
Kruppel-Like Factor 4
0
Kruppel-Like Transcription Factors
0
MIRN135 microRNA, human
0
MicroRNAs
0
NF-kappa B
0
Tff1 protein, mouse
0
Trefoil Factor-1
0
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
264-274Subventions
Organisme : NCI NIH HHS
ID : R01 CA077955
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA177372
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA116087
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA093999
Pays : United States
Organisme : BLRD VA
ID : IK6 BX003787
Pays : United States
Organisme : BLRD VA
ID : I01 BX001179
Pays : United States
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