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茉莉酸甲酯通过肿瘤坏死因子受体1降低乳腺癌细胞的膜流动性并诱导细胞凋亡。

Methyl jasmonate decreases membrane fluidity and induces apoptosis through tumor necrosis factor receptor 1 in breast cancer cells.

作者信息

Yeruva Laxmi, Elegbede John Abiodun, Carper Stephen W

机构信息

Chemistry Department, University of Nevada, Las Vegas, Nevada, USA.

出版信息

Anticancer Drugs. 2008 Sep;19(8):766-76. doi: 10.1097/CAD.0b013e32830b5894.

DOI:10.1097/CAD.0b013e32830b5894
PMID:18690087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2745996/
Abstract

In recent years, studies with plant compounds have shown both chemotherapeutic and chemopreventive properties. This study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. cis-Jasmone and methyl jasmonate (MJ) inhibited the long-term proliferation of MDA-MB-435 and MCF-7 cells. Cell cycle analysis showed G0/G1 and S-phase arrest with increasing apoptotic population. Cellular signaling studies with MJ showed decreased membrane fluidity and activation of extrinsic and intrinsic apoptotic pathways. Specifically in extrinsic apoptotic pathway increased expression of TNF receptor 1, activation of mitogen-activated protein kinase and caspase-8 was observed. MJ also decreased the mitochondrial membrane potential and activated caspase-3 in breast cancer cells. In conclusion our results revealed novel-signaling mechanism of MJ in breast cancer cells, indicating that MJ could have potential applications for chemotherapeutic purposes.

摘要

近年来,对植物化合物的研究已显示出其化疗和化学预防特性。这项针对植物应激激素(茉莉酸酯)的研究表明其对乳腺癌细胞具有生长抑制作用。顺式茉莉酮和茉莉酸甲酯(MJ)抑制了MDA-MB-435和MCF-7细胞的长期增殖。细胞周期分析显示,随着凋亡细胞数量增加,细胞停滞在G0/G1期和S期。对MJ进行的细胞信号传导研究表明,细胞膜流动性降低,外源性和内源性凋亡途径被激活。具体而言,在外源性凋亡途径中,观察到肿瘤坏死因子受体1表达增加、丝裂原活化蛋白激酶和半胱天冬酶-8被激活。MJ还降低了乳腺癌细胞的线粒体膜电位并激活了半胱天冬酶-3。总之,我们的结果揭示了MJ在乳腺癌细胞中的新信号传导机制,表明MJ可能具有潜在的化疗应用价值。

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