三氧化二砷通过FoxO3a抑制乳腺癌血管生成的体外实验

发布时间：2018-04-25 09:23

本文选题：三氧化二砷 + 乳腺癌　；参考：《南京医科大学学报(自然科学版)》2017年07期

【摘要】：目的:研究三氧化二砷(As_2O_3)对乳腺癌肿瘤血管生成的影响,并初步探讨其可能的分子机制。方法:以人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)为实验对象,制备肿瘤条件培养基模拟肿瘤微环境培养细胞。使用不同浓度的As_2O_3(0、4、8μmol/L)处理HUVECs细胞后,通过划痕试验检测内皮细胞迁移能力,Matrigel试验检测内皮细胞体外小管形成情况,CCK-8法检测细胞的增殖情况,Annexin V染色检测细胞凋亡,Western blot检测蛋白表达。结果:与对照组相比,As_2O_3处理组细胞的迁移及小管形成能力明显下降;细胞增殖活性降低,凋亡增加;细胞中FoxO3a蛋白及其下游Fas-L、p27Kip1蛋白的表达增多。结论:As_2O_3可以通过上调FoxO3a的蛋白表达水平,激活其下游通路,抑制血管内皮细胞的增殖,促进其凋亡,并降低其体外血管形成能力,提示As_2O_3可能在抑制乳腺癌血管生成中起重要作用。
[Abstract]:Aim: to study the effect of arsenic trioxide (as _ S _ 2O _ 3) on the angiogenesis of breast cancer and its possible molecular mechanism. Methods: human umbilical vein endothelial cells were cultured in human umbilical vein endothelial cells (HUVECs). After treating HUVECs cells with different concentrations of as _ 2O _ 3 / L _ (48 渭 mol / L), The migration ability of endothelial cells was detected by scratch test and Matrigel test was used to detect the formation of tubules in vitro. The proliferation of endothelial cells was detected by CCK-8 method and the expression of apoptosis protein was detected by Annexin V staining. Results: compared with the control group, the ability of migration and tubule formation was decreased, the cell proliferation activity was decreased and apoptosis was increased, and the expression of FoxO3a protein and Fas-LP27Kip1 protein was increased. Conclusion as _ S _ 2O _ 3 can up-regulate the expression of FoxO3a protein, activate its downstream pathway, inhibit the proliferation of vascular endothelial cells, promote its apoptosis, and decrease its ability of angiogenesis in vitro. The results suggest that As_2O_3 may play an important role in inhibiting angiogenesis in breast cancer.
【作者单位】：徐州医科大学基础医学院病理学教研室;
【基金】：国家自然科学基金(81372479,81502387) 江苏省普通高校研究生科研创新课题(KYLX15_1476)
【分类号】：R737.9

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