Class I-Histone Deacetylase (HDAC) Inhibition is Superior to pan-HDAC Inhibition in Modulating Cisplatin Potency in High Grade Serous Ovarian Cancer Cell Lines.
Antineoplastic Agents
/ pharmacology
Antineoplastic Combined Chemotherapy Protocols
/ pharmacology
Apoptosis
Benzamides
/ pharmacology
Cell Line, Tumor
Cell Survival
Cisplatin
/ therapeutic use
Cystadenocarcinoma, Serous
/ drug therapy
Drug Synergism
Female
Histone Deacetylase Inhibitors
/ pharmacology
Histone Deacetylases
Humans
Hydroxamic Acids
/ pharmacology
Ovarian Neoplasms
/ drug therapy
Panobinostat
/ pharmacology
Phenylurea Compounds
/ pharmacology
Pyridines
/ pharmacology
antitumor platinum agents
caspase activity
cisplatin
combination treatment
entinostat
high grade serous ovarian cancer (HGSOC)
histone deacetylase inhibitors
nexturastat A
panobinostat
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
22 Jun 2019
22 Jun 2019
Historique:
received:
30
05
2019
revised:
19
06
2019
accepted:
20
06
2019
entrez:
26
6
2019
pubmed:
27
6
2019
medline:
21
1
2020
Statut:
epublish
Résumé
High grade serous ovarian cancer (HGSOC) is the most common and aggressive ovarian cancer subtype with the worst clinical outcome due to intrinsic or acquired drug resistance. Standard treatment involves platinum compounds. Cancer development and chemoresistance is often associated with an increase in histone deacetylase (HDAC) activity. The purpose of this study was to examine the potential of HDAC inhibitors (HDACi) to increase platinum potency in HGSOC. Four HGSOC cell lines with different cisplatin sensitivity were treated with combinations of cisplatin and entinostat (class I HDACi), panobinostat (pan-HDACi), or nexturastat A (class IIb HDACi), respectively. Inhibition of class I HDACs by entinostat turned out superior in increasing cisplatin potency than pan-HDAC inhibition in cell viability assays (MTT), apoptosis induction (subG1), and caspase 3/7 activation. Entinostat was synergistic with cisplatin in all cell lines in MTT and caspase activation assays. MTT assays gave combination indices (CI values) < 0.9 indicating synergism. The effect of HDAC inhibitors could be attributed to the upregulation of pro-apoptotic genes (
Identifiants
pubmed: 31234549
pii: ijms20123052
doi: 10.3390/ijms20123052
pmc: PMC6627993
pii:
doi:
Substances chimiques
4-((1-butyl-3-phenylureido)methyl)-N-hydroxybenzamide
0
Antineoplastic Agents
0
Benzamides
0
Histone Deacetylase Inhibitors
0
Hydroxamic Acids
0
Phenylurea Compounds
0
Pyridines
0
entinostat
1ZNY4FKK9H
Panobinostat
9647FM7Y3Z
Histone Deacetylases
EC 3.5.1.98
Cisplatin
Q20Q21Q62J
Types de publication
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : INST 208/690-1
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