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Transcriptome Analysis Reveals HgCl2 Induces Apoptotic Cell Death in Human Lung Carcinoma H1299 Cells through Caspase-3-Independent Pathway

机译:转录组分析显示HgCl2通过Caspase-3独立的途径诱导人肺癌H1299细胞中的凋亡细胞死亡

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摘要

Mercury is one of the detrimental toxicants that can be found in the environment and exists naturally in different forms; inorganic and organic. Human exposure to inorganic mercury, such as mercury chloride, occurs through air pollution, absorption of food or water, and personal care products. This study aimed to investigate the effect of HgCl2 on cell viability, cell cycle, apoptotic pathway, and alters of the transcriptome profiles in human non-small cell lung cancer cells, H1299. Our data show that HgCl2 treatment causes inhibition of cell growth via cell cycle arrest at G0/G1- and S-phase. In addition, HgCl2 induces apoptotic cell death through the caspase-3-independent pathway. Comprehensive transcriptome analysis using RNA-seq indicated that cellular nitrogen compound metabolic process, cellular metabolism, and translation for biological processes-related gene sets were significantly up- and downregulated by HgCl2 treatment. Interestingly, comparative gene expression patterns by RNA-seq indicated that mitochondrial ribosomal proteins were markedly altered by low-dose of HgCl2 treatment. Altogether, these data show that HgCl2 induces apoptotic cell death through the dysfunction of mitochondria.
机译:汞是在环境中可以发现的有害毒物之一,并以不同的形式存在;无机和有机。通过空气污染,食物或水,以及个人护理产品,人们接触无机汞,例如汞氯化汞。该研究旨在探讨HGCL2对人非小细胞肺癌细胞H1299中转录组谱的细胞活力,细胞周期,凋亡途径和改变的影响。我们的数据表明,HGCl2治疗导致通过G0 / G1和S相管通过细胞周期停滞抑制细胞生长。此外,HGCL2通过Caspase-3无关的途径诱导凋亡细胞死亡。使用RNA-SEQ的综合转录组分析表明,通过HGCl2治疗显着上调了细胞氮化合物的代谢过程,细胞代谢和用于生物过程相关基因集的翻译。有趣的是,RNA-SEQ的比较基因表达模式表明,线粒体核糖体蛋白通过低剂量的HGCl2处理显着改变。总的来说,这些数据显示HGCL2通过线粒体功能障碍诱导凋亡细胞死亡。

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