芥酸通过上调 TRPM2 通道增加顺铂诱导的结直肠癌细胞死亡和氧化应激的效力。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Ayşenur Nazıroğlu, Ahmet Çarhan, Mustafa Nazıroğlu
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引用次数: 0

摘要

芥酸(ErA)是欧米茄-9 单不饱和脂肪酸的一种来源。ErA 可导致肿瘤细胞凋亡和氧化应激,具有抗肿瘤作用,但 HT-29 人类结直肠癌细胞系除外。线粒体 Ca2+ 和 Zn2+ 积累会产生活性自由氧(ROS),进而激活 TRPM2,从而触发肿瘤细胞的凋亡和 Ca2+ 信号通路。我们将细胞分为五组:对照组、ErA 组(200 µM,48 小时)、CSP 组(25 µM,24 小时)和 ErA + CSP + TRPM2 拮抗剂组(200 µM 香芹酚和 25 µM N-(对戊基肉桂酰)蒽二酸,24 小时)。TRPM2 拮抗剂降低了 ErA 和 CSP 诱导的 H2O2-诱导的细胞内游离 Ca2+ 浓度([Ca2+]c)和二磷酸腺苷核糖诱导的 TRPM2 电流的增加。研究发现,ErA 和 CSP 通过提高细胞内游离 Zn2+ 浓度(Zn2+]c)、caspase-3、-8 和 -9、线粒体膜功能障碍和 ROS,同时降低还原型谷胱甘肽、细胞活力和细胞数量,导致细胞凋亡和细胞死亡。通过激活TRPM2,ErA介导的进入线粒体的[Ca2+]c和Zn2+]c增加,从而增强了CSP对细胞的氧化、凋亡和肿瘤细胞死亡效应。 总之,我们观察到,通过激活TRPM2,ErA和CSP联合治疗HT-29肿瘤细胞具有协同作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Erucic acid increases the potency of cisplatin-induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel

Erucic acid (ErA) is a source of omega-9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT-29 human colorectal cancer cell line. The apoptotic and Ca2+ signaling pathways in tumor cells are triggered when mitochondrial Ca2+ and Zn2+ accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2. ErA-induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin (CSP). We aimed to study the effects of ErA and CSP incubations on ROS, apoptosis, and cell death in the HT-29 cells by activating TRPM2. The cells were divided into five groups: control, ErA (200 µM for 48 h), CSP (25 µM for 24 h), and ErA + CSP + TRPM2 antagonists (200 µM carvacrol and 25 µM N-(p-amylcinnamoyl)anthranilic acid for 24 h). The TRPM2 antagonists reduced ErA plus CSP-induced increases in H2O2-induced intracellular free Ca2+ concentration ([Ca2+]c) and adenosine diphosphate-ribose-caused TRPM2 currents. ErA and CSP were found to cause apoptosis and cell death by raising the intracellular free Zn2+ concentration (Zn2+]c), caspase-3, −8, and −9, mitochondrial membrane dysfunction, and ROS, while lowering reduced glutathione, cell viability, and cell number. The oxidative, apoptotic, and tumor cell death effects of CSP in the cells were enhanced by the increase of ErA-mediated [Ca2+]c and Zn2+]c entering mitochondria through the activation of TRPM2. In conclusion, we observed that the combination of ErA and CSP was synergistic via TRPM2 activation for the treatment of HT-29 tumor cells.

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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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