Temozolomide Induces Senescence and Repression of DNA Repair Pathways in Glioblastoma Cells via Activation of ATR-CHK1, p21, and NF-κB.
Animals
Antineoplastic Agents, Alkylating
/ pharmacology
Apoptosis
Ataxia Telangiectasia Mutated Proteins
/ genetics
Cell Cycle
Cell Proliferation
Cellular Senescence
Checkpoint Kinase 1
/ genetics
Cyclin-Dependent Kinase Inhibitor p21
/ genetics
DNA Methylation
DNA Repair
/ drug effects
DNA Repair Enzymes
/ antagonists & inhibitors
Female
Gene Expression Regulation, Neoplastic
Glioblastoma
/ drug therapy
Humans
Mice
Mice, Inbred BALB C
Mice, Nude
NF-kappa B
/ genetics
Temozolomide
/ pharmacology
Tumor Cells, Cultured
Xenograft Model Antitumor Assays
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
01 01 2019
01 01 2019
Historique:
received:
11
06
2018
revised:
07
09
2018
accepted:
22
10
2018
pubmed:
27
10
2018
medline:
23
10
2019
entrez:
27
10
2018
Statut:
ppublish
Résumé
The DNA-methylating drug temozolomide, which induces cell death through apoptosis, is used for the treatment of malignant glioma. Here, we investigate the mechanisms underlying the ability of temozolomide to induce senescence in glioblastoma cells. Temozolomide-induced senescence was triggered by the specific DNA lesion O
Identifiants
pubmed: 30361254
pii: 0008-5472.CAN-18-1733
doi: 10.1158/0008-5472.CAN-18-1733
doi:
Substances chimiques
Antineoplastic Agents, Alkylating
0
CDKN1A protein, human
0
Cyclin-Dependent Kinase Inhibitor p21
0
NF-kappa B
0
ATR protein, human
EC 2.7.11.1
Ataxia Telangiectasia Mutated Proteins
EC 2.7.11.1
CHEK1 protein, human
EC 2.7.11.1
Checkpoint Kinase 1
EC 2.7.11.1
DNA Repair Enzymes
EC 6.5.1.-
Temozolomide
YF1K15M17Y
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
99-113Informations de copyright
©2018 American Association for Cancer Research.