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Melatonin triggers autophagic cell death by regulating RORC in Hodgkin lymphoma.

褪黑素通过调节霍奇金淋巴瘤的 RORC 触发自噬性细胞死亡。

  • 影响因子:3.78
  • DOI:10.1016/j.biopha.2020.109811
  • 作者列表:"Yan G","Lei H","He M","Gong R","Wang Y","He X","Li G","Pang P","Li X","Yu S","Du W","Yuan Y
  • 发表时间:2020-03-01
Abstract

Melatonin (Mel) has been shown to involve in many essential cell functions via modulating many signaling pathways. We for the first time investigated that Mel exerted anti-tumor activities in Hodgkin lymphoma (HL) via inhibiting cell proliferation and promoting cell apoptosis. Further study revealed that Mel treatment increased expression of LC3-II and decreased p62 proteins with the enhanced production of autolysosome, indicating it induced activation of autophagy. Nevertheless, Mel treatment together with autophagy inhibitors 3-MA or CQ exacerbated the damage effect of Mel in HL cells, which means autophagy plays a protective role in this process. Furthermore, we found Mel treatment increased the expression of G protein-coupled receptors MT2 and retinoic acid-related orphan receptors (RORs), eg. RORA, RORB and RORC. While RORC has the highest increase in Mel treated HL cells. In addition, RORC overexpression induced autophagy activation. Therefore, Mel showed tumor-suppressive role due to an increased level of RORC induced autophagy in HL.

摘要

褪黑素 (Melatonin,Mel) 已被证明通过调节许多信号通路参与许多必需的细胞功能。我们首次研究了 Mel 通过抑制细胞增殖和促进细胞凋亡而在霍奇金淋巴瘤 (HL) 中发挥抗肿瘤活性。进一步研究发现,Mel 处理增加了 LC3-II 的表达,减少了 p62 蛋白的表达,同时增加了自溶酶体的产生,表明其诱导了自噬的激活。尽管如此,Mel 与自噬抑制剂 3-MA 或 CQ 一起处理加剧了 Mel 在 HL 细胞中的损伤效应,这意味着自噬在此过程中发挥了保护作用。此外,我们发现 Mel 治疗增加了 G 蛋白偶联受体 MT2 和维甲酸相关孤儿受体 (ror) 的表达,例如。RORA 、 rob 和 RORC。而 RORC 在 Mel 处理的 HL 细胞中增加最高。此外,RORC 过表达诱导自噬激活。因此,Mel 由于 RORC 诱导的 HL 自噬水平升高而表现出肿瘤抑制作用。

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关键词: 暂无
翻译标题与摘要 下载文献
影响因子:3.78
发表时间:2020-03-01
DOI:10.1016/j.biopha.2020.109811
作者列表:["Yan G","Lei H","He M","Gong R","Wang Y","He X","Li G","Pang P","Li X","Yu S","Du W","Yuan Y"]

METHODS:Melatonin (Mel) has been shown to involve in many essential cell functions via modulating many signaling pathways. We for the first time investigated that Mel exerted anti-tumor activities in Hodgkin lymphoma (HL) via inhibiting cell proliferation and promoting cell apoptosis. Further study revealed that Mel treatment increased expression of LC3-II and decreased p62 proteins with the enhanced production of autolysosome, indicating it induced activation of autophagy. Nevertheless, Mel treatment together with autophagy inhibitors 3-MA or CQ exacerbated the damage effect of Mel in HL cells, which means autophagy plays a protective role in this process. Furthermore, we found Mel treatment increased the expression of G protein-coupled receptors MT2 and retinoic acid-related orphan receptors (RORs), eg. RORA, RORB and RORC. While RORC has the highest increase in Mel treated HL cells. In addition, RORC overexpression induced autophagy activation. Therefore, Mel showed tumor-suppressive role due to an increased level of RORC induced autophagy in HL.

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