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首页> 外文期刊>Journal of cellular physiology. >Involvement of Bid in the crosstalk between ferroptotic agent‐induced ER stress and TRAIL‐induced apoptosis
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Involvement of Bid in the crosstalk between ferroptotic agent‐induced ER stress and TRAIL‐induced apoptosis

机译:Bid 参与铁蛋白试剂诱导的 ER 应激和 TRAIL 诱导的细胞凋亡之间的串扰

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Abstract Tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) induces death receptor‐mediated extrinsic apoptosis, specifically in cancer cells, and Bid (BH3‐interacting domain death agonist) plays an important role in TRAIL‐induced apoptosis. Ferroptosis is a newly defined form of regulated cell death known to be distinct from other forms of cell death. However, our previous studies have shown that ferroptosis shares common pathways with other types of programmed cell death such as apoptosis. In this study, we investigated the role of Bid in the crosstalk between the ferroptotic agent‐induced endoplasmic reticulum (ER) stress response and TRAIL‐induced apoptosis. When human colorectal carcinoma HCT116 cells were treated with the ferroptosis‐inducing agents artesunate and erastin in combination with TRAIL, TRAIL‐induced activation of caspase‐8 was enhanced, and subsequently, the truncation of Bid was increased. Similar results were observed when ovarian adenocarcinoma OVCAR‐3 cells were treated with the ferroptotic agents in combination with TRAIL. Results from studies with Bid mutants reveal that the truncation of Bid and the presence of intact BH3 domains are critical for synergistic apoptosis. Nonfunctional Bid mutants were not able to activate the mitochondria‐dependent apoptosis pathway, which is required for the conversion of p19 to p17, the active form of caspase‐3. These results indicate that Bid plays a critical role in the crosstalk between the ferroptotic agent‐induced ER stress response and TRAIL‐induced apoptosis.
机译:摘要肿瘤坏死因子相关细胞凋亡诱导配体(TRAIL)导致死亡受体介导的外在应承担的细胞凋亡,特别是在癌症细胞,报价(BH3量相互作用域死亡受体激动剂)扮演重要的角色在TRAIL诱导细胞凋亡。Ferroptosis是一种新定义的规范细胞死亡是有别于其他形式的细胞死亡。表明ferroptosis股票共同通路与其他类型的细胞程序性死亡等细胞凋亡。角色之间的串扰ferroptotic剂诱导内质网(ER)应激反应和小道诱导细胞凋亡。当人类大肠癌癌HCT116细胞与代理ferroptosis检测诱导治疗青蒿琥酯和erastin结合,小道还是诱导激活半胱天冬酶8增强,随后,截断的报价是增加了。卵巢腺癌OVCAR 3细胞治疗结合ferroptotic代理线索。显示,收购和截断存在完整的BH3领域至关重要协同细胞凋亡。无法激活线粒体高依赖的细胞凋亡途径在哪个需要转换的p19 p17,活动形式的半胱天冬酶3。,在相声中起着至关重要的作用ferroptotic代理之间诱导ER应激响应和TRAIL诱导细胞凋亡。

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