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Bufadienolide compounds sensitize human breast cancer cells to TRAIL-induced apoptosis via inhibition of STAT3/Mcl-1 pathway
Dong, Yinhui1; Yin, Shutao1; Li, Jinghua1; Jiang, Cheng2; Ye, Min3; Hu, Hongbo1
关键词Bufadienolides TRAIL Apoptosis Breast cancer cells Mcl-1
刊名APOPTOSIS
2011-04-01
DOI10.1007/s10495-011-0573-5
16期:4页:394-403
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]HEPATOCELLULAR-CARCINOMA ; BUFALIN ; GROWTH ; DEATH ; MECHANISMS ; RESISTANCE ; EXPRESSION ; CHEMOTHERAPY ; INVOLVEMENT ; ACTIVATION
英文摘要

The death receptor ligand TRAIL is considered a promising candidate for cancer therapy because of its preferential toxicity to malignant cells. However its efficacy has been challenged by a number of resistance mechanisms. Therefore, agents that can overcome the resistance to enhance therapeutic efficacy of TRAIL are needed. In the current study, we found that bufalin, bufotalin and gamabufotalin, key members of bufadienolides isolated from a traditional Chinese medicine ChanSu, significantly potentiated human breast cancer cells with different status of ER-alpha to apoptosis induction of TRAIL, as evidenced by enhanced Annexin V/FITC positive cells (apoptotic cells), cytoplasmic histone-associated-DNA-fragments, membrane permeability transition (MPT), caspases activation and PARP cleavage. Further mechanistic investigation demonstrated that bufalin was able to significantly decrease Mcl-1 expression and modestly decrease Bcl-XL expression level. Down-regulations of these anti-apoptotic proteins were well correlated with inhibition of transcription factor STAT3 activation. The important consequence of down-regulation Mcl-1 in the enhancement action by combining bufalin with TRAIL was confirmed by either knockdown or overexpression of Mcl-1 approach. Our findings for the first time provided strong evidences that bufadienolide compounds have excellent potential to be developed as a novel class of sensitizers of TRAIL.

语种英语
WOS记录号WOS:000288954900007
项目编号2009-2-11 ; 31071533 ; 30972172
资助机构Chinese Universities Scientific Fund ; National Natural Science Foundation of China (NSFC)
引用统计
被引频次:39[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64146
专题北京大学药学院
北京大学药学院_天然药物学系
作者单位1.China Agr Univ, Div Nutr & Hlth, Coll Food Sci & Nutr Engn, Beijing 100083, Peoples R China
2.Univ Minnesota, Hormel Inst, Austin, MN 55912 USA
3.Peking Univ, Hlth Sci Ctr, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
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GB/T 7714
Dong, Yinhui,Yin, Shutao,Li, Jinghua,et al. Bufadienolide compounds sensitize human breast cancer cells to TRAIL-induced apoptosis via inhibition of STAT3/Mcl-1 pathway[J]. APOPTOSIS,2011,16(4):394-403.
APA Dong, Yinhui,Yin, Shutao,Li, Jinghua,Jiang, Cheng,Ye, Min,&Hu, Hongbo.(2011).Bufadienolide compounds sensitize human breast cancer cells to TRAIL-induced apoptosis via inhibition of STAT3/Mcl-1 pathway.APOPTOSIS,16(4),394-403.
MLA Dong, Yinhui,et al."Bufadienolide compounds sensitize human breast cancer cells to TRAIL-induced apoptosis via inhibition of STAT3/Mcl-1 pathway".APOPTOSIS 16.4(2011):394-403.
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