Department of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Bioinformatics Core, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Environ Mol Mutagen. 2021 Mar;62(3):216-226. doi: 10.1002/em.22428. Epub 2021 Mar 2.
Restriction of the sulfur amino acids methionine and cysteine has recently been proposed as potential adjuvant therapy in cancer. While cysteine depletion has been associated with ferroptotic cell death, methionine depletion has not. We hypothesized that comparing the response of melanoma cell lines to depletion of the amino acids methionine and cysteine would give us insight into the critical role in cancer of these two closely related amino acids. We analyzed the response to three conditions: methionine depletion, methionine replacement with homocysteine, and cysteine depletion. In cancer cells, the transcription factor ATF4 was induced by all three tested conditions. The replacement of methionine with homocysteine produced a strong ferroptotic gene signature. We also detected an activation of the NRF2 antioxidant pathway by both methionine and cysteine depletion. Total glutathione levels were decreased by 42% in melanoma cells grown without methionine, and by 95% in cells grown without cysteine. Lipid peroxidation was increased in cells grown without cysteine, but not in cells grown without methionine. Despite the large degree of overlap in gene expression between methionine and cysteine depletion, methionine depletion and replacement of methionine with homocysteine was associated with apoptosis while cysteine depletion was associated with ferroptosis. Glutamine depletion produced comparable gene expression patterns and was associated with a 28% decrease in glutathione. Apoptosis was detected in these cells. In this experiment, a strong ATF4-driven ferroptotic gene signature was insufficient to induce ferroptosis without a concomitant profound decrease in glutathione levels.
最近有人提出,限制蛋氨酸和半胱氨酸等含硫氨基酸可能是癌症的辅助治疗方法。虽然半胱氨酸耗竭与铁死亡细胞死亡有关,但蛋氨酸耗竭并非如此。我们假设比较黑素瘤细胞系对氨基酸蛋氨酸和半胱氨酸耗竭的反应,将使我们深入了解这两种密切相关的氨基酸在癌症中的关键作用。我们分析了对三种条件的反应:蛋氨酸耗竭、蛋氨酸用同型半胱氨酸替代以及半胱氨酸耗竭。在癌细胞中,三种测试条件均诱导转录因子 ATF4 的表达。用同型半胱氨酸替代蛋氨酸会产生强烈的铁死亡基因特征。我们还发现,蛋氨酸和半胱氨酸耗竭均激活了 NRF2 抗氧化途径。在没有蛋氨酸的情况下,黑素瘤细胞的总谷胱甘肽水平降低了 42%,在没有半胱氨酸的情况下降低了 95%。在没有半胱氨酸的情况下,细胞内脂质过氧化增加,但在没有蛋氨酸的情况下则没有增加。尽管蛋氨酸耗竭和半胱氨酸耗竭之间的基因表达有很大的重叠,但蛋氨酸耗竭和用同型半胱氨酸替代蛋氨酸与细胞凋亡有关,而半胱氨酸耗竭与铁死亡有关。谷氨酰胺耗竭产生了类似的基因表达模式,并与谷胱甘肽水平下降 28%有关。在这些细胞中检测到了细胞凋亡。在这项实验中,强烈的 ATF4 驱动的铁死亡基因特征不足以在不伴随谷胱甘肽水平显著降低的情况下诱导铁死亡。