CK1δ as a potential therapeutic target to treat bladder cancer.
Apoptosis
/ drug effects
Casein Kinase Idelta
/ antagonists & inhibitors
Cell Cycle
/ drug effects
Cell Line, Tumor
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Gene Expression Regulation, Neoplastic
/ drug effects
Gene Knockdown Techniques
Humans
Pyrimidines
/ pharmacology
Up-Regulation
/ drug effects
Urinary Bladder Neoplasms
/ genetics
CK1δ
apoptosis
bladder cancer
migration
necroptosis
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
13 04 2020
13 04 2020
Historique:
received:
16
11
2019
accepted:
27
01
2020
pubmed:
14
4
2020
medline:
11
5
2021
entrez:
14
4
2020
Statut:
ppublish
Résumé
Bladder cancer is the second most common genitourinary malignancy in the world. However, only immune-checkpoint inhibitors and erdafitinib are available to treat advanced bladder cancer. Our previous study reported that 4-((4-(4-ethylpiperazin-1-yl) phenyl)amino)-N-(3,4,5-trichlorophenyl)-7H-pyrrolo-[2, 3-d]pyrimidine-7-carboxamide hydrochloride (13i HCl) is a potent CK1δ inhibitor showing significant anti-bladder cancer activity. In this study, we elucidated the pharmacological mechanisms underlying 13i HCl's inhibition of human bladder cancer. Our results demonstrate that expression of the
Identifiants
pubmed: 32282334
pii: 102966
doi: 10.18632/aging.102966
pmc: PMC7185098
doi:
Substances chimiques
Pyrimidines
0
Casein Kinase Idelta
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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