Niclosamide-induced Wnt signaling inhibition in colorectal cancer is mediated by autophagy.
Autophagy
/ drug effects
Autophagy-Related Protein-1 Homolog
/ antagonists & inhibitors
Colorectal Neoplasms
/ drug therapy
Dishevelled Proteins
/ genetics
Frizzled Receptors
/ genetics
HCT116 Cells
HEK293 Cells
Humans
Intracellular Signaling Peptides and Proteins
/ antagonists & inhibitors
Mechanistic Target of Rapamycin Complex 1
/ antagonists & inhibitors
Neoplasm Proteins
/ antagonists & inhibitors
Niclosamide
/ pharmacology
Wnt Signaling Pathway
/ drug effects
beta Catenin
/ genetics
Wnt signaling
autophagy
biomarker
colorectal cancer
niclosamide
Journal
The Biochemical journal
ISSN: 1470-8728
Titre abrégé: Biochem J
Pays: England
ID NLM: 2984726R
Informations de publication
Date de publication:
08 02 2019
08 02 2019
Historique:
received:
23
05
2018
revised:
21
12
2018
accepted:
11
01
2019
pubmed:
13
1
2019
medline:
24
10
2019
entrez:
13
1
2019
Statut:
epublish
Résumé
The Wnt signaling pathway, known for regulating genes critical to normal embryonic development and tissue homeostasis, is dysregulated in many types of cancer. Previously, we identified that the anthelmintic drug niclosamide inhibited Wnt signaling by promoting internalization of Wnt receptor Frizzled 1 and degradation of Wnt signaling pathway proteins, Dishevelled 2 and β-catenin, contributing to suppression of colorectal cancer growth
Identifiants
pubmed: 30635359
pii: BCJ20180385
doi: 10.1042/BCJ20180385
pmc: PMC6643999
mid: NIHMS1041669
doi:
Substances chimiques
DVL1 protein, human
0
Dishevelled Proteins
0
FZD1 protein, human
0
Frizzled Receptors
0
Intracellular Signaling Peptides and Proteins
0
Neoplasm Proteins
0
beta Catenin
0
Niclosamide
8KK8CQ2K8G
Autophagy-Related Protein-1 Homolog
EC 2.7.11.1
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
ULK1 protein, human
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
535-546Subventions
Organisme : NCI NIH HHS
ID : K12 CA100639
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA172570
Pays : United States
Informations de copyright
© 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.
Références
Bioorg Med Chem. 2017 Mar 15;25(6):1804-1816
pubmed: 28233680
PLoS One. 2009 Sep 22;4(9):e7124
pubmed: 19771169
Nat Cell Biol. 2011 Feb;13(2):132-41
pubmed: 21258367
Am J Physiol Gastrointest Liver Physiol. 2010 Aug;299(2):G293-300
pubmed: 20508156
Bioorg Med Chem. 2018 Nov 1;26(20):5435-5442
pubmed: 30274939
Cell Signal. 2018 Jan;41:89-96
pubmed: 28389414
Breast Cancer Res. 2015 Feb 15;17:20
pubmed: 25849870
Nature. 2012 Jul 18;487(7407):330-7
pubmed: 22810696
Nature. 1999 Dec 9;402(6762):672-6
pubmed: 10604474
J Biol Chem. 2012 May 18;287(21):17530-45
pubmed: 22474287
Bioorg Med Chem. 2015 Sep 1;23(17):5829-38
pubmed: 26272032
Biomolecules. 2017 Jul 07;7(3):
pubmed: 28686223
Cancer Res. 2014 Jun 15;74(12):3238-47
pubmed: 24755471
Nat Rev Drug Discov. 2014 Jul;13(7):513-32
pubmed: 24981364
Biochemistry. 2009 Nov 3;48(43):10267-74
pubmed: 19772353
J Cardiovasc Pharmacol Ther. 2010 Sep;15(3):220-30
pubmed: 20595626
Nat Rev Cancer. 2017 Sep;17(9):528-542
pubmed: 28751651
FEBS Lett. 2010 Apr 2;584(7):1287-95
pubmed: 20083114
Mol Cancer. 2017 Jul 6;16(1):116
pubmed: 28683746
Nanoscale. 2017 Aug 31;9(34):12709-12717
pubmed: 28828438
Nat Cell Biol. 2010 Aug;12(8):781-90
pubmed: 20639871
Nat Rev Mol Cell Biol. 2013 Dec;14(12):759-74
pubmed: 24201109
Cell Res. 2014 Jan;24(1):58-68
pubmed: 24296784
Cancer Res. 2011 Jun 15;71(12):4172-82
pubmed: 21531761
Cell. 2017 Jun 1;169(6):985-999
pubmed: 28575679
Bioorg Med Chem Lett. 2013 Apr 1;23(7):2187-91
pubmed: 23453073