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首页> 外文期刊>Journal of Inorganic Biochemistry: An Interdisciplinary Journal >Molecular mechanisms of apoptosis and cell selectivity of zinc dithiocarbamates functionalized with hydroxyethyl substituents
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Molecular mechanisms of apoptosis and cell selectivity of zinc dithiocarbamates functionalized with hydroxyethyl substituents

机译：羟乙基取代基官能化的二硫代氨基甲酸锌的细胞凋亡和细胞选择性的分子机制

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摘要

In the solid state each of three binuclear zinc dithiocarbamates bearing hydroxyethyl groups, {Zn[S2CN(R)CH2CH2OH](2)}(2) for R = iPr (1), CH2CH2OH (2), and Me (3), and an all alkyl species, [Zn(S2CNEt2)(2)](2) (4), features a centrosymmetric {ZnSCS}(2) core with a step topology; both 1 and 3 were isolated as monohydrates. All compounds were broadly cytotoxic, specifically against human cancer cell lines compared with normal cells, with greater potency than cisplatin. Notably, some selectivity were indicated with 2 being the most potent against human ovarian carcinoma cells (cisA2780), and 4 being more cytotoxic toward multidrug resistant human breast carcinoma cells (MCF-7R), human colon adenocarcinoma cells (HT-29), and human lung adenocarcinoma epithelial cells (A549). Based on human apoptosis PCR-array analysis, caspase activities, DNA fragmentation, cell apoptotic assays, intracellular reactive oxygen species (ROS) measurements and human topoisomerase I inhibition, induction of apoptosis in HT-29 cells is demonstrated via both extrinsic and intrinsic pathways. Compounds 2-4 activate the p53 gene while 1 activates both p53 and p73. Cell cycle arrest at the S and G(2)/M phases correlates with inhibition of HT-29 cell growth. Cell invasion is also inhibited by 1-4 which is correlated with down-regulation of NF-kappa B. (C) 2015 Elsevier Inc. All rights reserved.
机译：在固态下，三个带有羟乙基的双核二硫代氨基甲酸锌，{R [i [S2CN（R）CH2CH2OH]（2）}（2），R = iPr（1），CH2CH2OH（2）和Me（3），以及所有的烷基物质[Zn（S2CNEt2）（2）]（2）（4）均具有中心对称的{ZnSCS}（2）核，具有阶梯形拓扑; 1和3均被分离为一水合物。与正常细胞相比，所有化合物均具有广泛的细胞毒性，特别是针对人癌细胞系，具有比顺铂更大的效力。值得注意的是，显示出一些选择性，其中2对人卵巢癌细胞（cisA2780）最有效，4对多药耐药人乳腺癌细胞（MCF-7R），人结肠腺癌细胞（HT-29）和人肺腺癌上皮细胞（A549）。基于人类凋亡PCR阵列分析，半胱天冬酶活性，DNA片段化，细胞凋亡测定，细胞内活性氧（ROS）测量和人类拓扑异构酶I抑制，已通过外部和内在途径证明了HT-29细胞的凋亡诱导作用。化合物2-4激活p53基因，而化合物1激活p53和p73。在S和G（2）/ M期的细胞周期停滞与抑制HT-29细胞的生长有关。细胞侵袭也被1-4抑制，这与NF-κB的下调有关。（C）2015 Elsevier Inc.保留所有权利。

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