ARID1A
ATR inhibition
CRISPR/Cas9
HDAC inhibition
SWI/SNF-complex
germ cell tumors
mass spectrometry
molecular therapy
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
07 Apr 2020
07 Apr 2020
Historique:
received:
07
03
2020
revised:
25
03
2020
accepted:
06
04
2020
entrez:
11
4
2020
pubmed:
11
4
2020
medline:
11
4
2020
Statut:
epublish
Résumé
Germ cell tumors (GCTs) are the most common solid malignancies found in young men. Although they generally have high cure rates, metastases, resistance to cisplatin-based therapy, and late toxicities still represent a lethal threat, arguing for the need of new therapeutic options. In a previous study, we identified downregulation of the chromatin-remodeling SWI/SNF complex member ARID1A as a key event in the mode of action of the histone deacetylase inhibitor romidepsin. Additionally, the loss-of-function mutations re-sensitize different tumor types to various drugs, like EZH2-, PARP-, HDAC-, HSP90- or ATR-inhibitors. Thus, ARID1A presents as a promising target for synthetic lethality and combination therapy. In this study, we deciphered the molecular function of ARID1A and screened for the potential of two pharmacological ARID1A inhibitors as a new therapeutic strategy to treat GCTs. By CRISPR/Cas9, we generated
Identifiants
pubmed: 32272809
pii: cancers12040905
doi: 10.3390/cancers12040905
pmc: PMC7226530
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Düsseldorf School of Oncology (DSO)
ID : Funding of BMFZ Mass Spectrometry
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