GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.
GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.
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DOI：
10.1016/j.cytogfr.2016.09.001
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发表时间：
2017-02
影响因子：
13
通讯作者：
Kalvakolanu DV
中科院分区：
文献类型：
--
作者：
Nallar SC;Kalvakolanu DV
细胞因子根据环境诱导细胞增殖或生长抑制。越来越清楚的是，标准放疗和/或化疗根除实体瘤的成功取决于IFN信号传导。在这篇综述中，我们讨论了肿瘤生长抑制的分子机制，在我们的实验室分离的基因产物，使用全基因组表达敲低策略。类维生素A干扰素诱导死亡相关基因-19（GRIM-19）通过拮抗癌蛋白发挥非典型肿瘤抑制因子的作用。作为线粒体呼吸链的组分，GRIM-19影响癌细胞中“瓦尔堡效应”的程度，因为许多晚期和/或侵袭性肿瘤显示严重下调的GRIM-19水平。此外，GRIM-19似乎在小鼠模型中调节先天性和获得性免疫应答。因此，GRIM-19位于有利于细胞保护和/或防止异常细胞生长的节点处。
Cytokines induce cell proliferation or growth suppression depending on the context. It is increasingly becoming clear that success of standard radiotherapy and/or chemotherapeutics to eradicate solid tumors is dependent on IFN signaling. In this review we discuss the molecular mechanisms of tumor growth suppression by a gene product isolated in our laboratory using a genome-wide expression knock-down strategy. Gene associated with retinoid-IFN-induced mortality −19 (GRIM-19) functions as non-canonical tumor suppressor by antagonizing oncoproteins. As a component of mitochondrial respiratory chain, GRIM-19 influences the degree of “Warburg effect” in cancer cells as many advanced and/or aggressive tumors show severely down-regulated GRIM-19 levels. In addition, GRIM-19 appears to regulate innate and acquired immune responses in mouse models. Thus, GRIM-19 is positioned at nodes that favor cell protection and/or prevent aberrant cell growth.