蟾毒灵通过重新分布乳腺癌细胞脂筏中的死亡受体增强TRAIL诱导的细胞凋亡。
Bufalin enhances TRAIL-induced apoptosis by redistributing death receptors in lipid rafts in breast cancer cells.
作者信息
Yan Shunchao, Qu Xiujuan, Xu Ling, Che Xiaofang, Ma Yanju, Zhang Lingyun, Teng Yuee, Zou Huawei, Liu Yunpeng
机构信息
aDepartment of Medical Oncology, The First Hospital of China Medical University bDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
出版信息
Anticancer Drugs. 2014 Jul;25(6):683-9. doi: 10.1097/CAD.0000000000000095.
Studies have shown that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in cancer cells. However, breast cancer cells are generally resistant to TRAIL. In the present study, we explored the effect of bufalin on TRAIL-induced breast cancer cell apoptosis. The results showed that bufalin enhanced TRAIL-induced apoptosis in MCF-7 and MDA-MB-231 breast cancer cells by activating the extrinsic apoptotic pathway. Bufalin also promoted the clustering of death receptor 4 (DR4) and DR5 in aggregated lipid rafts. The cholesterol-sequestering agent methyl-β-cyclodextrin reversed the DR4 and DR5 clustering and reduced bufalin+TRAIL-induced apoptosis. Overall, these results indicate that bufalin enhanced TRAIL-induced apoptosis in breast cancer cells by the partial redistribution of DRs in lipid rafts.
研究表明，肿瘤坏死因子相关凋亡诱导配体（TRAIL）可选择性诱导癌细胞凋亡。然而，乳腺癌细胞通常对TRAIL具有抗性。在本研究中，我们探究了蟾毒灵对TRAIL诱导的乳腺癌细胞凋亡的影响。结果显示，蟾毒灵通过激活外源性凋亡途径增强了TRAIL诱导的MCF-7和MDA-MB-231乳腺癌细胞凋亡。蟾毒灵还促进了死亡受体4（DR4）和DR5在聚集的脂筏中的聚集。胆固醇螯合剂甲基-β-环糊精逆转了DR4和DR5的聚集，并减少了蟾毒灵+TRAIL诱导的凋亡。总体而言，这些结果表明，蟾毒灵通过脂筏中死亡受体的部分重新分布增强了TRAIL诱导的乳腺癌细胞凋亡。
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