BET inhibitors repress expression of interferon-stimulated genes and synergize with HDAC inhibitors in glioblastoma.
Olga GusyatinerPierre BadyMinh D T PhamYvonne LeiJungyeon ParkRoy T DanielMauro DelorenziMonika E HegiPublished in: Neuro-oncology (2021)
Our approach identified BETi-induced vulnerabilities in cancer-relevant pathways, potentially amenable to synergistic combinatorial therapy, such as combination with HDACi. The direct inhibitory effect of BETi on IFN-responsive genes in GBM cells, including CD274, indicates modulation of the tumor immune landscape and warrants further studies.
Keyphrases
- genome wide
- induced apoptosis
- dendritic cells
- cancer therapy
- papillary thyroid
- poor prognosis
- bioinformatics analysis
- genome wide identification
- cell cycle arrest
- high glucose
- immune response
- diabetic rats
- dna methylation
- oxidative stress
- stem cells
- signaling pathway
- histone deacetylase
- drug delivery
- endoplasmic reticulum stress
- squamous cell carcinoma
- cell proliferation
- smoking cessation
- pi k akt
- replacement therapy