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Abstract：
Cancer is one of the deadliest human diseases, causing high rates of illness and death. Lung cancer has the highest mortality rate among all malignancies worldwide. Effusanin B, a diterpenoid derived from Isodon serra, showed therapeutic potential in treating non-small-cell lung cancer (NSCLC). Further research on the mechanism indicated that effusanin B inhibited the proliferation and migration of A549 cells both in vivo and in vitro. The in vitro activity assay demonstrated that effusanin B exhibited significant anticancer activity. Effusanin B induced apoptosis, promoted cell cycle arrest, increased the production of reactive oxygen species (ROS), and altered the mitochondrial membrane potential (MMP). Based on mechanistic studies, effusanin B was found to inhibit the proliferation and migration of A549 cells by affecting the signal transducer and activator of transcription 3 (STAT3) and focal adhesion kinase (FAK) pathways. Moreover, effusanin B inhibited tumor growth and spread in a zebrafish xenograft model and demonstrated anti-angiogenic effects in a transgenic zebrafish model.
摘要：
癌症是人类最致命的疾病之一,导致高发病率和死亡率。肺癌在全世界所有恶性肿瘤中死亡率最高。EffusaninB,一种来自Isodonserra的二萜，在治疗非小细胞肺癌（NSCLC）方面具有治疗潜力。进一步的机制研究表明，在体内和体外，吐露素B抑制A549细胞的增殖和迁移。体外活性测定表明，吐露素B具有明显的抗癌活性。EffusaninB诱导细胞凋亡，促进细胞周期停滞，增加活性氧（ROS）的产生，并改变了线粒体膜电位（MMP）。基于机械研究，发现EffusaninB通过影响信号转导和转录激活因子3（STAT3）和粘着斑激酶（FAK）途径来抑制A549细胞的增殖和迁移。此外，effusaninB在斑马鱼异种移植模型中抑制肿瘤生长和扩散，并在转基因斑马鱼模型中显示出抗血管生成作用。
