CCN1 suppresses cell proliferation of esophageal squamous cell carcinoma through amyloid precursor protein without DR6 participation.
APP
CCN1
Cell growth
DR6
Esophageal cancer
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
29
03
2022
revised:
24
05
2022
accepted:
26
05
2022
pubmed:
3
6
2022
medline:
18
6
2022
entrez:
2
6
2022
Statut:
ppublish
Résumé
Esophageal cancer is commonly seen as either squamous cell carcinoma (ESCC) or adenocarcinoma (EAC), two very different cancers. CCN1 is a matricellular protein that induces apoptosis in EAC cells through upregulation of DR5, a death receptor, while its role in ESCC is unclear. DR6 is another death receptor, which has been reported to induce apoptosis, necroptosis, or pyroptosis in various cell systems with or without the engagement of its putative ligand amyloid precursor protein (APP). In this study, we found that CCN1 and DR6 were both highly expressed in ESCC but downregulated in EAC. Overexpression of CCN1 in ESCC cells inhibited cell proliferation through upregulation of APP and its association with p53 without DR6 involvement. Overexpression of APP stopped cell growth, but overexpression of DR6 did not affect cell growth or cell death whatsoever.
Identifiants
pubmed: 35654297
pii: S0898-6568(22)00136-X
doi: 10.1016/j.cellsig.2022.110374
pii:
doi:
Substances chimiques
Amyloid beta-Protein Precursor
0
Receptors, Death Domain
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
110374Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.