ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
3-Acetyl-11-keto-β-boswellic acid (AKBA) induced antiproliferative effect by suppressing Notch signaling pathway and synergistic interaction with cisplatin against prostate cancer cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Deubiquitination of NICD1 by USP10 Restrains Esophageal Cancer: A Link Between NOTCH1 Stabilization, Oxidative Stress, and Ferroptosis.Neoplasia (New York, N.Y.) · 2026Article
- Recent Advances in Boswellic Acids as Anticancer Agents: Therapeutic Effects, SAR, and Computational Approaches.Current topics in medicinal chemistry · 2026Review
- Phytochemicals in overcoming venetoclax resistance in acute myeloid leukemia: mechanistic insights and therapeutic potential.Annals of hematology · 2025Review
- Synergistic Induction of Apoptosis by Boswellic Acid and Cisplatin in A549 Lung Cancer Cells Through NF-κB Modulation and p53 Pathway Activation.Current issues in molecular biology · 2025Article
- Xingxiao Pill Suppressed the Progression of Non-Small Cell Lung Cancer by Targeting SREBP1/FASN-Induced Fatty Acid Biosynthesis via PI3K/AKT/mTOR Signaling Pathway.Cancer management and research · 2025Article
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Abstract
Studies on the assessment of anticancer efficacy of plant-derived phytochemicals by targeting signaling pathways have drawn a lot of attention recently for human health. Multiple investigations have proposed an involvement of Notch pathway in the processes of cancer angiogenesis and metastasis, and drug resistance. Moreover, overexpression of Notch signaling is associated with increased prostate cancer (PrCa) cell growth and development. A number of chemotherapeutic agents are reported to become resistant over a period of time and have severe side effects. To increase efficacy and lessen drug-induced toxicity, a variety of bioactive compounds have been utilized alone or as adjuncts to traditional chemotherapy. Therefore, in the present study, the potential of AKBA in inhibiting the proliferation of PrCa cells by modulating Notch signaling components and its efficacy in combination with cisplatin was investigated. The results exhibited a substantial reduction in cell survival (IC50 = 25.28 µM at 24 h and 16.50 µM at 48 h) and cellular alterations in AKBA-treated PrCa cells. Additionally, AKBA caused nuclear condensation, increased reactive oxygen species (ROS) generation, mitochondrial membrane depolarization, and caspase activation, ultimately leading to apoptosis in PrCa cells. Moreover, AKBA-elicited apoptosis was evidenced by an augmentation in the Bax to Bcl2 ratio. AKBA was also found to induce G0/G1 arrest which was substantiated by reduced cyclin D1 and CDK4 expression levels concomitantly with increased expression of p21 and p27 genes. Intriguingly, AKBA demonstrated significant downregulation of Notch signaling mediators. Furthermore, the isobolograms of the combination treatment indicated that AKBA has the potential to synergistically enhance the cytotoxic efficacy of cisplatin in DU145 cells, as evidenced by CI < 1 across all tested combinations. Overall, the results of this study suggest strong antiproliferative, apoptotic, and chemo-sensitizing potential of AKBA. Thus, AKBA holds a promising drug candidature warranting further investigation as a probable therapeutic option for both the prevention and treatment of PrCa and other solid tumors.
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