Epigenetic preconditioning with decitabine sensitizes glioblastoma to temozolomide via induction of MLH1.
Chemosensitization
DNA methylation
Decitabine
Glioblastoma
Mismatch repair
Temozolomide
Journal
Journal of neuro-oncology
ISSN: 1573-7373
Titre abrégé: J Neurooncol
Pays: United States
ID NLM: 8309335
Informations de publication
Date de publication:
May 2020
May 2020
Historique:
received:
22
01
2020
accepted:
14
03
2020
pubmed:
21
3
2020
medline:
16
3
2021
entrez:
21
3
2020
Statut:
ppublish
Résumé
To improve the standard treatment paradigm for glioblastoma (GBM), efforts have been made to explore the efficacy of epigenetic agents as chemosensitizers. Recent data suggest possible synergy between decitabine (DAC), a DNA hypomethylating agent, and temozolomide (TMZ) in GBM, but the mechanism remains unclear. The objective of this study was to determine the effects of DAC on TMZ sensitization in a consecutively derived set of primary GBM cultures, with a focus on mismatch repair (MMR) proteins. Half maximal inhibitory concentrations (IC TMZ IC DAC enhances TMZ cytotoxicity in a subset of GBM cell lines, comprising lines both MGMT methylated and unmethylated tumors. This effect may be driven by levels of MLH1 via E2F1 transcription factor binding. Using unbiased long-range next-generation bisulfite-sequencing, we identified a region of the proximal MLH1 promoter with differential methylation patterns that has potential utility as a clinical biomarker for TMZ sensitization.
Identifiants
pubmed: 32193690
doi: 10.1007/s11060-020-03461-4
pii: 10.1007/s11060-020-03461-4
pmc: PMC7256087
doi:
Substances chimiques
Antineoplastic Agents
0
MLH1 protein, human
0
Decitabine
776B62CQ27
MutL Protein Homolog 1
EC 3.6.1.3
Temozolomide
YF1K15M17Y
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
557-566Références
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