AN N-terminal Smac peptide sensitizes human prostate carcinoma cells to methyl jasmonate-induced apoptosis
AN N-terminal Smac peptide sensitizes human prostate carcinoma cells to methyl jasmonate-induced apoptosis
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AN N 末端 Smac 肽使人前列腺癌细胞对茉莉酸甲酯诱导的细胞凋亡敏感
DOI：
10.1016/j.canlet.2010.12.009
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发表时间：
2011-03-01
期刊：
影响因子：
9.7
通讯作者：
Zeng, Fuqing
中科院分区：
文献类型：
--
作者：
Jiang, Guosong;Zhao, Jun;Zeng, Fuqing
尽管抗癌剂茉莉酸甲酯(MJ)已被证明选择性地针对恶性肿瘤细胞，而不针对正常细胞，但激素耐药的前列腺癌细胞比其他癌细胞对MJ具有相对抗药性。在本研究中，我们研究了Smac细胞通透性七个残基多肽(SmacN7)对MJ诱导的细胞凋亡的影响。SmacN7显著增强MJ对人前列腺癌细胞的生长抑制作用，但对近端肾小管上皮细胞无明显影响。此外，SmacN7通过caspase-9依赖和非依赖途径敏化MJ诱导的细胞凋亡。因此，阻断癌细胞中过度表达的IAP可能在茉莉酸类药物化疗中产生潜在的治疗益处。(C)2010爱思唯尔爱尔兰有限公司。保留所有权利。
Although the anti-cancer agent methyl jasmonate (MJ) has been shown to selectively target malignant cells while sparing normal ones, hormone-refractory prostate cancer cells are relatively resistant to MJ than other cancer cells. In the present study, we investigated the effect of cell permeable seven-residue peptide of Smac (SmacN7), an antagonist of the inhibitor of apoptosis proteins (IAPs), on MJ-induced apoptosis. SmacN7 significantly enhanced the growth inhibition effect of MJ in human prostate cancer cells, but not in proximal tubular epithelial cells. Moreover, SmacN7 sensitizes MJ-induced apoptosis through both caspase-9-dependent and -independent pathways. Thus, blockade of the over-expressed IAPs in cancer cells could yield a potential therapeutic benefit in jasmonates-based chemotherapy. (C) 2010 Elsevier Ireland Ltd. All rights reserved.