中文摘要：

Cucurbitacin B (崽) ，从 Cucurbitaceae 植物孤立的 triterpenoid 混合物，作为一个有希望的反癌症代理人被报导了，还它的行动机制仍然是争论的。在这研究，我们在鼠科的 B16F10 黑瘤房间探索了崽的潜在的机制。反增长和反侵略效果在有教养的房间被估计，并且在 vivo 反肿瘤，活动在一个鼠科的下的黑瘤模型被评估。流动 cytometry 被采用分析细胞周期分发和反应的氧种(ROS ) 层次。肌动朊层次被西方的污点分析决定，并且微分表示蛋白质的侧面被一条量的 proteomic 途径识别。结果证明那崽在房间增长，殖民地形成，以及移植和黑瘤房间的侵略潜力上施加了禁止的效果。下的黑瘤的生长显著地在当时，与崽对待的老鼠被禁止与控制相比组。而且，崽治疗引起了快速的房间膜 blebbing 和变丑，并且导致了 G2/M-phase 拘捕和 multiploid 房间的形成。尤其是， G 肌动朊水池很快被弄空，肌动朊总数在崽处理以后快速被形成。很多细胞骨架规章的蛋白质是调整的差别。ROS 生产的阻塞显著地减少了 G 肌动朊弄空能力和崽的反肿瘤活动。这些调查结果显示那崽在黑瘤房间通过 ROS 依赖的肌动朊聚集导致 G 肌动朊水池的快速的弄空，它可以部分至少说明它的反肿瘤活动。

英文摘要：

Cucurbitacin B （CUB）, a triterpenoid compound isolated from Cucurbitaceae plants, has been reported as a promising anti-cancer agent, yet its action mechanism is still controversial. In this study, we explored the potential mechanism of CuB in murine B16F10 melanoma cells. Anti-proliferation and antMnvasion effects were assessed in cultured cells, and in vivo anti-tumor activity was eval- uated in a murine subcutaneous melanoma model. Flow cytometry was adopted to analyze cell cycle distribution and reactive oxygen species （ROS） levels. Actin levels were determined by western blot analysis, and the profiles of differential expressed proteins were identified by a quantitative proteomic approach. The results showed that CuB exerted inhibitory effects on cell proliferation, colony formation, as well as migration and invasion potential of the melanoma cells. The growth of subcutaneous melanoma was significantly inhibited in mice treated with CuB when compared with control group. Furthermore, CuB treatment caused rapid cell membrane blebbing and deformation, and induced G2/M-phase arrest and formation of multiploid cells. Notably, the G-actin pool was rapidly depleted and actin aggregates were formed quickly after CuB treatment. A number of cytoskeleton-regulatory proteins were differentially regulated. Blockage of ROS production significantly reduced the G-actin depletion ability and the anti-tumor activity of CuB. These findings indicate that CuB induces rapid depletion of the G-actin pool through ROS-dependent actin aggregation in melanoma cells, which may at least partly account for its anti-tumor activity.