Korsnes Mónica Suárez, Korsnes Reinert
Department of Chemistry, Biotechnology and Food Science, Norwegian University of Life SciencesÅs, Norway.
Nofima ASÅs, Norway.
Front Cell Dev Biol. 2017 Mar 31;5:30. doi: 10.3389/fcell.2017.00030. eCollection 2017.
The marine toxin yessotoxin (YTX) can cause various cytotoxic effects depending on cell type and cell line. It is well known to trigger distinct mechanisms for programmed cell death which may overlap or cross-talk. The present contribution provides the first evidence that YTX can cause genotoxicity and induce mitotic catastrophe which can lead to different types of cell death. This work also demonstrates potential information gain from non-intrusive computer-based tracking of many individual cells during long time. Treatment of BC3H1 cells at their exponential growth phase causes atypical nuclear alterations and formation of giant cells with multiple nuclei. These are the most prominent morphological features of mitotic catastrophe. Giant cells undergo slow cell death in a necrosis-like manner. However, apoptotic-like cell death is also observed in these cells. Electron microscopy of treated BC3H1 cells reveal uncondensed chromatin and cells with double nuclei. Activation of p-p53, p-H2AX, p-Chk1, p-ATM, and p-ATR and down-regulation of p-Chk2 indicate DNA damage response and cell cycle deregulation. Micronuclei formation further support this evidence. Data from tracking single cells reveal that YTX treatment suppresses a second round of cell division in BC3H1 cells. These findings suggest that YTX can induce genomic alterations or imperfections in chromosomal segregation leading to permanent mitotic failure. This understanding extends the list of effects from YTX and which are of interest to control cancer and tumor progression.
海洋毒素岩沙海葵毒素(YTX)可根据细胞类型和细胞系引发各种细胞毒性效应。众所周知,它会触发程序性细胞死亡的不同机制,这些机制可能会重叠或相互作用。本研究首次提供证据表明,YTX可导致基因毒性并诱导有丝分裂灾难,进而导致不同类型的细胞死亡。这项工作还证明了通过长时间对许多单个细胞进行非侵入性计算机跟踪可能获得的信息。在指数生长期处理BC3H1细胞会导致非典型核改变并形成多核巨细胞。这些是有丝分裂灾难最显著的形态学特征。巨细胞以类似坏死的方式经历缓慢的细胞死亡。然而,在这些细胞中也观察到了类似凋亡的细胞死亡。对处理过的BC3H1细胞进行电子显微镜检查发现染色质未浓缩且细胞具有双核。p-p53、p-H2AX、p-Chk1、p-ATM和p-ATR的激活以及p-Chk2的下调表明存在DNA损伤反应和细胞周期失调。微核形成进一步支持了这一证据。对单个细胞的跟踪数据表明,YTX处理会抑制BC3H1细胞的第二轮细胞分裂。这些发现表明,YTX可诱导基因组改变或染色体分离缺陷,导致永久性有丝分裂失败。这一认识扩展了YTX的影响范围,对控制癌症和肿瘤进展具有重要意义。