Ovarian cancer progression is driven by epigenetic dysregulation and constitutive activation of oncogenic signaling pathways. In particular, aberrant JAK/STAT3 signaling promotes tumor growth, survival, and angiogenesis through transcriptional regulation of targets such as VEGFA, while SOCS proteins act as negative regulators. Histone deacetylase (HDAC) inhibitors show antitumor activity in ovarian cancer, but the interplay between SOCS-mediated STAT3 regulation and angiogenic signaling remains incompletely understood. This study aims to define how epigenetic modulation by dacinostat disrupts STAT3-driven oncogenic and angiogenic pathways through SOCS1/3 regulation, thereby providing mechanistic insight into its therapeutic potential in ovarian cancer. Human ovarian cancer SKOV3 cells were treated with the pan-HDAC inhibitor dacinostat (LAQ824). Cell viability and proliferation were assessed by MTT assays and real-time live-cell imaging. Cell cycle distribution and apoptosis were analyzed by flow cytometry and confocal microscopy. Long-term survival was evaluated by colony formation assays. Intracellular ROS levels and DNA damage were measured by DCFDA staining and γH2AX immunocytochemistry, respectively. Protein expression and pathway modulation were examined by Western blotting. Antitumor efficacy in vivo was tested in a SKOV3 xenograft model in BALB/c nude mice treated with intraperitoneal dacinostat. Dacinostat significantly reduced SKOV3 cell viability and proliferation, induced S-phase arrest, and promoted apoptosis. Treatment elevated ROS levels, triggered DNA damage marked by γH2AX accumulation, and impaired clonogenic survival. Mechanistically, dacinostat upregulated SOCS1 and SOCS3, leading to suppression of STAT3 phosphorylation and downregulation of VEGFA expression. In vivo, dacinostat treatment markedly inhibited tumor growth in SKOV3 xenograft-bearing mice, consistent with the in vitro findings. Pan-HDAC inhibition by dacinostat exerts potent antitumor effects in ovarian cancer by inducing oxidative DNA damage, promoting apoptosis, and suppressing STAT3-driven oncogenic and angiogenic signaling via SOCS1/3 upregulation. These results provide mechanistic insight into epigenetic regulation of STAT3 signaling and support dacinostat as a promising therapeutic strategy for ovarian cancer.