斑蝥素抑制人高转移卵巢癌细胞HO-8910PM侵袭转移的体外实验研究

背景与目的:斑蝥素在治疗癌症方面显示出其独特的疗效,已有较多文献证实核因子鄄κB(nuclearfactor鄄kappaB,NF鄄资B)与肿瘤侵袭转移关系密切。本研究旨在观察斑蝥素对人高转移卵巢癌细胞HO鄄8910PM转移相关能力的影响,并探讨其作用机理。方法:MTT法及细胞粘附人工重组基底膜实验检测斑蝥素对HO鄄8910PM细胞的细胞毒作用及粘附能力的影响;用Transwell小室法检测斑蝥素对HO鄄8910PM细胞侵袭能力和趋化运动能力的影响;Westernblot法分析斑蝥素对HO鄄8910PM细胞中NF鄄κB和血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)的影响。结果:20μmol/L的斑蝥素作用6h对HO鄄8910PM细胞抑制率及体外侵袭、趋化运动和粘附的抑制率分别为(8.4±2.2)%及(38.8±1.7)%、(40.3±5.6)%和(55.1±6.7)%。20μmol/L斑蝥素能明显下调HO鄄8910PM细胞中NF鄄κB和VEGF的表达。结论:斑蝥素能抑制HO鄄8910PM细胞的侵袭、运动和粘附能力。斑蝥素抗肿瘤侵袭转移的作用机制与NF鄄κB和VEGF蛋白的表达下调有关。

Inhibitory effect of cantharidin on invasion and metastasis of highly metastatic ovarian carcinoma cell line HO-8910PM

BACKGROUND & OBJECTIVE: Cantharidin, a natural toxin, has specific antitumor actions. Many researches confirmed that nuclear factor-kappaB (NF-kappaB) closely relates with invasion and metastasis of tumor. This study was designed to investigate inhibitory effect of cantharidin on metastasis-related ability of human highly metastatic ovarian carcinoma cell line HO-8910PM, and its mechanism. METHODS: MTT assay was used to examine cytotoxicity of cantharidin on HO-8910PM cells. Effect of cantharidin on adhesion potential of HO-8910PM cells was tested by cell-Matrigel adhesion assay. Transwell chamber assay was performed to determine its effect on invasion and migration capacities of HO-8910PM cells. Protein levels of NF-kappaB P65 subunit and vascular endothelial growth factor (VEGF) were assessed by Western blot. RESULTS: After 6-h treatment of 20 micromol/L of cantharidin, inhibitory rate of HO-8910PM cells was (8.4+/-2.2)%, inhibitory rates of invasion, migration, and adhesion capacities of HO-8910PM cells were (38.8+/-1.7)%, (40.3+/-5.6)%, and (55.1+/-6.7)%, respectively; protein levels of NF-kappaB P65 subunit and VEGF were down-regulated. CONCLUSIONS: Cantharidin can inhibit migration, invasion, and adhesion of HO-8910PM cells. Its possible mechanism may be involved in down-regulations of NF-kappaB P65 subunit and VEGF.