
The study shows that the HDAC inhibitor belinostat boosts Bim, Puma, and Noxa expression, suppresses Bcl-xL, and induces apoptosis in SKOV3 and IGROV1-R10 ovarian cancer cells. Belinostat’s efficacy was amplified by co-targeting Bcl-xL or Mcl-1, including in patient-derived organoids. These findings highlight a promising combination strategy leveraging belinostat to overcome resistance and improve ovarian cancer treatment.
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