ACSL3-PAI-1 signaling axis mediates tumor-stroma cross-talk promoting pancreatic cancer progression.
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
26
03
2020
accepted:
15
09
2020
entrez:
31
10
2020
pubmed:
1
11
2020
medline:
15
4
2022
Statut:
epublish
Résumé
Pancreatic ductal adenocarcinoma (PDAC) is characterized by marked fibrosis and low immunogenicity, features that are linked to treatment resistance and poor clinical outcomes. Therefore, understanding how PDAC regulates the desmoplastic and immune stromal components is of great clinical importance. We found that acyl-CoA synthetase long-chain 3 (ACSL3) is up-regulated in PDAC and correlates with increased fibrosis. Our in vivo results show that
Identifiants
pubmed: 33127675
pii: 6/44/eabb9200
doi: 10.1126/sciadv.abb9200
pmc: PMC7608806
pii:
doi:
Substances chimiques
Plasminogen Activator Inhibitor 1
0
Serpin E2
0
Serpine2 protein, mouse
0
Acsl3 protein, mouse
EC 6.1.2.3
Coenzyme A Ligases
EC 6.2.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).
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