海洋天然产物为药物开发提供了巨大的潜力，但海洋生物的有限供应带来了重大挑战。建立水产养殖业是应对这一挑战的可持续解决方案，可促进活性成分的大规模生产，同时减少我们对野生种群的依赖和对当地环境的危害。为了充分利用水产养殖作为生物活性产品的来源，我们利用水产养殖珊瑚的提取物建立了一个无细胞系统，以具有蛋白质调节活性的分子成分为目标，包括拓扑异构酶 II、HDAC 和微管蛋白聚合。随后进行了体外研究，包括 MTT 测定、流式细胞术、共聚焦显微镜和蛋白质印迹以及体内异种移植模型，以验证活性提取物的功效并进一步阐明其细胞毒性机制。使用 NGS 和基因修饰技术阐明了调节蛋白。进行分子对接和 SwissADME 测定来评估小分子的药物相似性、药代动力学和药物化学相关特性。 Lobophytum crassum (LCE) 提取物表现出强大的广谱活性，对微管蛋白聚合具有显着抑制作用，并且对前列腺癌细胞显示出较低的 IC50 值。流式细胞术和蛋白质印迹分析表明，LCE 诱导细胞凋亡，凋亡蛋白裂解的 caspase-3 表达增加以及早期和晚期凋亡细胞群的表达增加证明了这一点。在异种移植肿瘤实验中，LCE显着抑制肿瘤生长并减少肿瘤体积（PC3：43.9％；Du145：49.2％）和重量（PC3：48.8％；Du145：7.8％）。此外，LCE 抑制前列腺癌细胞迁移和侵袭，上调上皮标记物 E-钙粘蛋白并抑制 EMT 相关蛋白。此外，LCE 有效减弱 PC3 和 Du145 细胞中 TGF-β 诱导的 EMT。生物活性引导的分馏和SwissADME验证证实，LCE的主要成分13-乙酰氧基sarcocrassolide (13-AC)在抗癌药物的开发方面具有更大的潜力。

Marine natural products offer immense potential for drug development, but the limited supply of marine organisms poses a significant challenge. Establishing aquaculture presents a sustainable solution for this challenge by facilitating the mass production of active ingredients while reducing our reliance on wild populations and harm to local environments. To fully utilize aquaculture as a source of biologically active products, a cell-free system was established to target molecular components with protein-modulating activity, including topoisomerase II, HDAC, and tubulin polymerization, using extracts from aquaculture corals. Subsequent in vitro studies were performed, including MTT assays, flow cytometry, confocal microscopy, and Western blotting, along with in vivo xenograft models, to verify the efficacy of the active extracts and further elucidate their cytotoxic mechanisms. Regulatory proteins were clarified using NGS and gene modification techniques. Molecular docking and SwissADME assays were performed to evaluate the drug-likeness and pharmacokinetic and medicinal chemistry-related properties of the small molecules. The extract from Lobophytum crassum (LCE) demonstrated potent broad-spectrum activity, exhibiting significant inhibition of tubulin polymerization, and showed low IC50 values against prostate cancer cells. Flow cytometry and Western blotting assays revealed that LCE induced apoptosis, as evidenced by the increased expression of apoptotic protein-cleaved caspase-3 and the populations of early and late apoptotic cells. In the xenograft tumor experiments, LCE significantly suppressed tumor growth and reduced the tumor volume (PC3: 43.9%; Du145: 49.2%) and weight (PC3: 48.8%; Du145: 7.8%). Additionally, LCE inhibited prostate cancer cell migration, and invasion upregulated the epithelial marker E-cadherin and suppressed EMT-related proteins. Furthermore, LCE effectively attenuated TGF-β-induced EMT in PC3 and Du145 cells. Bioactivity-guided fractionation and SwissADME validation confirmed that LCE's main component, 13-acetoxysarcocrassolide (13-AC), holds greater potential for the development of anticancer drugs.