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

机译:茉莉酸甲酯降低了膜的流动性并通过肿瘤坏死因子受体1诱导了乳腺癌细胞的凋亡

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摘要

In recent years, studies with plant compounds have shown both chemotherapeutic and chemopreventive properties. The current study with plant stress hormones (jasmonates) showed growth inhibitory effects in breast cancer cells. Cis-jasmone (CJ) 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 TNFR1, activation of MAPK 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.
机译:近年来,对植物化合物的研究显示了化学治疗和化学预防性质。目前对植物胁迫激素(茉莉酸酯)的研究显示了对乳腺癌细胞生长的抑制作用。顺式茉莉酮(CJ)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,随着凋亡人口的增加,G0 / G1和S期阻滞。用MJ进行的细胞信号研究表明,膜流动性降低以及外源和内在凋亡途径的激活。特别是在外在凋亡途径中,TNFR1的表达增加,观察到MAPK和caspase-8的激活。 MJ还降低了乳腺癌细胞中的线粒体膜电位和激活的caspase-3。总之,我们的研究结果揭示了MJ在乳腺癌细胞中的新型信号传导机制,表明MJ在化学治疗方面可能具有潜在的应用。

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