Targeting AHR Increases Pancreatic Cancer Cell Sensitivity to Gemcitabine through the ELAVL1-DCK Pathway.
AHR
DCK
ELAVL1
HMOX1
PDAC
gemcitabine
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
24 Aug 2023
24 Aug 2023
Historique:
received:
18
07
2023
revised:
21
08
2023
accepted:
22
08
2023
medline:
11
9
2023
pubmed:
9
9
2023
entrez:
9
9
2023
Statut:
epublish
Résumé
The aryl hydrocarbon receptor (AHR) is a transcription factor that is commonly upregulated in pancreatic ductal adenocarcinoma (PDAC). AHR hinders the shuttling of human antigen R (ELAVL1) from the nucleus to the cytoplasm, where it stabilises its target messenger RNAs (mRNAs) and enhances protein expression. Among these target mRNAs are those induced by gemcitabine. Increased AHR expression leads to the sequestration of ELAVL1 in the nucleus, resulting in chemoresistance. This study aimed to investigate the interaction between AHR and ELAVL1 in the pathogenesis of PDAC in vitro.
Identifiants
pubmed: 37685961
pii: ijms241713155
doi: 10.3390/ijms241713155
pmc: PMC10487468
pii:
doi:
Substances chimiques
ELAV-Like Protein 1
0
ELAVL1 protein, human
0
Gemcitabine
0
Pancreatic Hormones
0
Receptors, Aryl Hydrocarbon
0
RNA, Messenger
0
Deoxycytidine Kinase
EC 2.7.1.74
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Financed from the funds of financial mechanism of the European Economic Area (EEA) States (Iceland and Liechtenstein) and Norway.
ID : Grant No. S-BMT-21-11 (LT08-2-LMT-K-01-060)
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