PI3K/AKT 通路的异常激活是前列腺癌发生的驱动因素。因此，抑制PI3K/AKT信号通路的功能是治疗前列腺癌的一种策略。 Ilicicolin C 是一种从珊瑚来源的真菌 Acremium scleotigenum GXIMD 02501 中分离出来的壳二氯素衍生物。具有抗炎活性，但其抗前列腺癌的活性尚未阐明。采用MTT法、平板克隆形成法、流式细胞仪和实时细胞分析技术检测伊利西林C对前列腺癌细胞活力、增殖、凋亡和迁移的影响。利用分子对接软件和表面等离子共振技术分析了ilicicolin C与PI3K/AKT蛋白之间的相互作用。进行蛋白质印迹分析以检查蛋白质表达的变化。最后利用QikProp软件模拟了ilicicolin C在体内的过程，并利用斑马鱼异种移植模型进一步验证了ilicicolin C的体内抗前列腺癌活性。 Ilicicolin C 对前列腺癌细胞具有细胞毒性作用，其中对 PC-3 细胞的作用最显着。 Ilicicolin C 抑制 PC-3 细胞的增殖和迁移。它还可以阻断细胞周期并诱导 PC-3 细胞凋亡。此外，ililicicolin C 可以与 PI3K/AKT 蛋白结合。此外，ilicicolin C 抑制 PI3K、AKT 和 mTOR 蛋白的表达，还可以调节 PI3K/AKT/mTOR 信号通路下游蛋白的表达。此外，计算推测，ilicicolin C 口服吸收良好，斑马鱼异种移植模型证实了 ilicicolin C 的体内抗前列腺癌作用。Ilicicolin C 成为一种有前途的海洋化合物，能够通过抵消PI3K/AKT/mTOR 的异常激活，表明 ilicicolin C 可能是抗前列腺癌药物开发的可行候选者。这些发现凸显了艾利西林 C 对抗前列腺癌的潜力，并阐明了其作用机制。© 2024。作者获得 Springer Science Business Media, LLC（Springer Nature 旗下公司）的独家许可。

Aberrant activation of the PI3K/AKT pathway is a driving factor in the development of prostate cancer. Therefore, inhibiting the function of the PI3K/AKT signaling pathway is a strategy for the treatment of prostate cancer. Ilicicolin C is an ascochlorin derivative isolated from the coral-derived fungus Acremonium sclerotigenum GXIMD 02501. Which has anti-inflammatory activity, but its activity against prostate cancer has not yet been elucidated. MTT assay, plate clone-formation assay, flow cytometry and real-time cell analysis technology were used to detect the effects of ilicicolin C on cell viability, proliferation, apoptosis and migration of prostate cancer cells. Molecular docking software and surface plasmon resonance technology were used to analyze the interaction between ilicicolin C and PI3K/AKT proteins. Western blot assay was performed to examine the changes in protein expression. Finally, QikProp software was used to simulate the process of ilicicolin C in vivo, and a zebrafish xenograft model was used to further verify the anti-prostate cancer activity of ilicicolin C in vivo. Ilicicolin C showed cytotoxic effects on prostate cancer cells, with the most significant effect on PC-3 cells. Ilicicolin C inhibited proliferation and migration of PC-3 cells. It could also block the cell cycle and induce apoptosis in PC-3 cells. In addition, ilicicolin C could bind to PI3K/AKT proteins. Furthermore, ilicicolin C inhibited the expression of PI3K, AKT and mTOR proteins and could also regulate the expression of downstream proteins in the PI3K/AKT/mTOR signaling pathway. Moreover, the calculations speculated that ilicicolin C was well absorbed orally, and the zebrafish xenograft model confirmed the in vivo anti-prostate cancer effect of ilicicolin C. Ilicicolin C emerges as a promising marine compound capable of inducing apoptosis of prostate cancer cells by counteracting the aberrant activation of PI3K/AKT/mTOR, suggesting that ilicicolin C may be a viable candidate for anti-prostate cancer drug development. These findings highlight the potential of ilicicolin C against prostate cancer and shed light on its mechanism of action.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.