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亚硒酸钠通过线粒体和溶酶体抑制耐药膀胱癌细胞的增殖和激活细胞死亡。

Suppression of proliferation and activation of cell death by sodium selenite involves mitochondria and lysosomes in chemoresistant bladder cancer cells.

机构信息

Department of Medical Biology and Genetics Charles University, Faculty of Medicine in Hradec Králové, Zborovská 2089, 500 03 Hradec Králové, Czech Republic.

Department of Medical Biology and Genetics Charles University, Faculty of Medicine in Hradec Králové, Zborovská 2089, 500 03 Hradec Králové, Czech Republic.

出版信息

J Trace Elem Med Biol. 2019 Mar;52:58-67. doi: 10.1016/j.jtemb.2018.11.009. Epub 2018 Nov 27.

Abstract

The specific effects of sodium selenite (selenite) on a chemoresistant human bladder cancer cell line RT-112/D21 were investigated during 72 h. Selenite at low concentration of 2.5 μmol (otherwise tolerated in normal urothelial cells UROtsa) suppressed growth and proliferation of the tested cancer cells via induced oxidative stress. Selenite further altered mitochondrial functions (i.e. decreased mitochondrial membrane potential, increased production of superoxide and reduced ATP synthesis), disrupted lysosomal membranes and activated autophagy. These changes in selenite-exposed cells ultimately resulted in their demise via necrosis and other cell death modality displaying heterotypic apoptotic and autophagic features.

摘要

研究了亚硒酸钠(硒代硫酸盐)在 72 小时内对化学抗性人膀胱癌细胞系 RT-112/D21 的具体影响。低浓度的 2.5μmol 硒代硫酸盐(在正常尿路上皮细胞 UROtsa 中可耐受)通过诱导氧化应激抑制了测试癌细胞的生长和增殖。硒代硫酸盐进一步改变了线粒体功能(即降低线粒体膜电位、增加超氧化物的产生和减少 ATP 合成),破坏了溶酶体膜并激活了自噬。暴露于硒代硫酸盐的细胞最终通过坏死和其他具有异质凋亡和自噬特征的细胞死亡方式死亡。

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