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<p>Ovarian cancer remains a highly lethal malignancy, largely driven by chemoresistance and the limited effectiveness of current therapeutic strategies. Ursolic acid (UA) and acetyl-11-keto-β-boswellic acid (AKBA) have shown anticancer activity in various models; however, their combined effects in chemoresistant ovarian cancer remain poorly understood. The synergistic anticancer potential of UA and AKBA was evaluated across multiple ovarian cancer cell models, including chemoresistant phenotypes, alongside non-malignant endothelial controls. Combined treatment reduced cell viability and increased apoptotic cell death, while maintaining selectivity toward malignant cells. A consistent G2/M-phase arrest was observed, suggesting disruption of cell-cycle progression. At the molecular level, these effects were associated with transcriptional modulation of key regulators of metabolism and survival signaling, along with factors involved in cell-cycle control. Treatment also induced metabolic disturbances, including depletion of ATP and glutathione, consistent with impaired energy balance and redox homeostasis, particularly in resistant models. Molecular docking analysis further supported the interaction of UA and AKBA with key apoptosis- and cell cycle–related targets, including Bcl-2 and CDK2. Overall, these findings suggest that the UA–AKBA combination may exert a multi-target anticancer effect in ovarian cancer, including chemoresistant models, and may represent a promising therapeutic approach.</p>

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Synergistic induction of apoptosis and metabolic reprogramming by ursolic acid and acetyl-11-keto-β-boswellic acid in chemoresistant ovarian cancer cell lines

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月29日

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  • Issa S. Al-Amri,
  • Samira Farhadi,
  • Abdulaziz Y. AlKindi,
  • Ahmed Al-Harrasi,
  • Sulaiman S. Al-Hashmi,
  • Waleed K. Al Rajhi,
  • Najeeb Ur Rehman,
  • Marwa A. Al-Riyami,
  • Khamis O. Al-Riyami,
  • Sausan Al-Yaqoobi

摘要

Ovarian cancer remains a highly lethal malignancy, largely driven by chemoresistance and the limited effectiveness of current therapeutic strategies. Ursolic acid (UA) and acetyl-11-keto-β-boswellic acid (AKBA) have shown anticancer activity in various models; however, their combined effects in chemoresistant ovarian cancer remain poorly understood. The synergistic anticancer potential of UA and AKBA was evaluated across multiple ovarian cancer cell models, including chemoresistant phenotypes, alongside non-malignant endothelial controls. Combined treatment reduced cell viability and increased apoptotic cell death, while maintaining selectivity toward malignant cells. A consistent G2/M-phase arrest was observed, suggesting disruption of cell-cycle progression. At the molecular level, these effects were associated with transcriptional modulation of key regulators of metabolism and survival signaling, along with factors involved in cell-cycle control. Treatment also induced metabolic disturbances, including depletion of ATP and glutathione, consistent with impaired energy balance and redox homeostasis, particularly in resistant models. Molecular docking analysis further supported the interaction of UA and AKBA with key apoptosis- and cell cycle–related targets, including Bcl-2 and CDK2. Overall, these findings suggest that the UA–AKBA combination may exert a multi-target anticancer effect in ovarian cancer, including chemoresistant models, and may represent a promising therapeutic approach.