Cx32 mediates norepinephrine-promoted EGFR-TKI resistance in a gap junction-independent manner in non-small-cell lung cancer.
Afatinib
/ pharmacology
Antineoplastic Agents
/ pharmacology
Carcinoma, Non-Small-Cell Lung
/ metabolism
Connexins
/ metabolism
Drug Resistance, Neoplasm
/ physiology
Gene Expression Regulation
/ physiology
Humans
Lung Neoplasms
/ metabolism
Norepinephrine
/ metabolism
Protein Kinase Inhibitors
/ pharmacology
Psychological Distress
Gap Junction beta-1 Protein
Afatinib
Cx32
NSCLC
drug resistance
norepinephrine
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
03
02
2019
revised:
07
05
2019
accepted:
09
05
2019
pubmed:
4
6
2019
medline:
13
6
2020
entrez:
2
6
2019
Statut:
ppublish
Résumé
The second-generation EGFR-TKI Afatinib is an irreversible ErbB family blocker used to treat patients with non-small-cell lung cancer (NSCLC). Unfortunately, resistance to this drug develops over time, and patients are always under great psychological pressure. A previous study showed that chronic stress hormones participate in EGFR-TKI resistance via β
Substances chimiques
Antineoplastic Agents
0
Connexins
0
Protein Kinase Inhibitors
0
Afatinib
41UD74L59M
Norepinephrine
X4W3ENH1CV
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
23146-23159Informations de copyright
© 2019 Wiley Periodicals, Inc.