Sulforaphane sensitizes human breast cancer cells to paclitaxel-induced apoptosis by downregulating the NF-κB signaling pathway

被引:32
作者
Kim, Seung-Hyun [1 ]
Park, Hyun-Jung [1 ]
Moon, Dong-Oh [1 ]
机构
[1] Daegu Univ, Dept Biol Educ, 201 Daegudae St, Gyongsan 38453, Gyeongsang, South Korea
关键词
sulforaphane; paclitaxel; apoptosis; BCL2; apoptosis regulator; nuclear factor kappa B; TUBULIN POLYMERIZATION; INHIBITION; TAXOL; PHOSPHORYLATION; OVEREXPRESSION; ACTIVATION; KINASE; DEATH;
D O I
10.3892/ol.2017.5950
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Sulforaphane (SFN), an isothiocyanate present in cruciferous vegetables, has been demonstrated to inhibit the growth of various types of cancer cell. The aim of the present study was to investigate whether SFN sensitizes breast cancer cells to paclitaxel-induced apoptosis and to identify the signal pathway through which SFN mediates apoptosis. Combined treatment of breast cancer cells with SFN and paclitaxel resulted in increased activation of apoptotic signaling pathway members, including caspase-3, -8 and -9, and cytochrome c, compared with treatment with SFN or paclitaxel alone. In addition, treatment with SFN and paclitaxel resulted in downregulation of the nuclear factor kappa B signaling pathway, and reduced protein expression of apoptosis regulator Bcl-2 and phosphorylated AKT serine/threonine kinase. Furthermore, SFN-paclitaxel-induced apoptosis was inhibited by overexpression of Bcl-2. The results of the present study suggest that combined treatment with SFN and paclitaxel is a novel therapeutic strategy for the treatment of breast cancer.
引用
收藏
页码:4427 / 4432
页数:6
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