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首页> 外文期刊>Apoptosis >An apoptosis targeted stimulus with nanosecond pulsed electric fields (nsPEFs) in E4 squamous cell carcinoma
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An apoptosis targeted stimulus with nanosecond pulsed electric fields (nsPEFs) in E4 squamous cell carcinoma

机译：纳秒脉冲电场（nsPEFs）对E4鳞状细胞癌的凋亡靶向刺激

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摘要

Stimuli directed towards activation of apoptosis mechanisms are an attractive approach to eliminate evasion of apoptosis, a ubiquitous cancer hallmark. In these in vitro studies, kinetics and electric field thresholds for several apoptosis characteristics are defined in E4 squamous carcinoma cells (SCC) exposed to ten 300 ns pulses with increasing electric fields. Cell death was >95% at the highest electric field and coincident with phosphatidylserine externalization, caspase and calpain activation in the presence and absence of cytochrome c release, decreases in Bid and mitochondria membrane potential (Δψm) without apparent changes reactive oxygen species levels or in Bcl2 and Bclxl levels. Bid cleavage was caspase-dependent (55–60%) and calcium-dependent (40–45%). Intracellular calcium as an intrinsic mechanism and extracellular calcium as an extrinsic mechanism were responsible for about 30 and 70% of calcium dependence for Bid cleavage, respectively. The results reveal electric field-mediated cell death induction and progression, activating pro-apoptotic-like mechanisms and affecting plasma membrane and intracellular functions, primarily through extrinsic-like pathways with smaller contributions from intrinsic-like pathways. Nanosecond second pulsed electric fields trigger heterogeneous cell death mechanisms in E4 SCC populations to delete them, with caspase-associated cell death as a predominant, but not an unaccompanied event.
机译：针对细胞凋亡机制的激活的刺激是消除细胞凋亡逃避的一种有吸引力的方法，这是普遍存在的癌症标志。在这些体外研究中，在暴露于十个300 ns脉冲且电场增加的E4鳞状癌细胞（SCC）中，定义了几种凋亡特征的动力学和电场阈值。在最高电场下细胞死亡> 95％，并与存在和不存在细胞色素c释放的磷脂酰丝氨酸外在化，胱天蛋白酶和钙蛋白酶激活同时发生，Bid和线粒体膜电位（Δψm）降低，而活性氧种类水平或Bcl2和Bclxl水平。出价切割取决于caspase（55-60％）和钙依赖（40-45％）。细胞内钙作为内在机制，细胞外钙作为外在机制，分别占Bid切割钙依赖性的30％和70％。结果显示电场介导的细胞死亡诱导和进展，激活促凋亡样机制并影响质膜和细胞内功能，主要是通过外源性途径，而内源性途径的贡献较小。纳秒秒脉冲电场触发E4 SCC群体中的异质细胞死亡机制以将其删除，而胱天蛋白酶相关的细胞死亡是主要事件，但并非无伴生事件。

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