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首页> 外文期刊>Cell cycle >CSN6 positively regulates c-Jun in a MEKK1-dependent manner
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CSN6 positively regulates c-Jun in a MEKK1-dependent manner

机译：CSN6以依赖MEKK1的方式正调控c-Jun

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摘要

c-Jun is a proto-oncoprotein that is commonly overexpressed in many types of cancer and is believed to regulate cell proliferation, the cell cycle, and apoptosis by controlling AP-1 activity. Understanding the c-Jun regulation is important to develop treatment strategy for cancer. The COP9 signalosome subunit 6 (CSN6) plays a critical role in ubiquitin-mediated protein degradation. MEKK1 is a serine/threonine kinase and E3 ligase containing PHD/RING domain involved in c-Jun ubiquitination. Here, we show that CSN6 associates with MEKK1 and reduces MEKK1 expression level by facilitating the ubiquitin-mediated degradation of MEKK1. Also we show that CSN6 overexpression diminishes MEKK1-mediated c-Jun ubiquitination, which is manifested in mitigating osmotic stress-mediated c-Jun downregulation. Thus, CSN6 is involved in positively regulating the stability of c-Jun. Overexpression of CSN6 correlates with the upregulation of c-Jun target gene expression in cancer. These findings provide new insight into CSN6-MEKK1-c-Jun axis in tumorigenesis.
机译：c-Jun是一种原癌蛋白，通常在许多类型的癌症中过表达，并且据信可以通过控制AP-1活性来调节细胞增殖，细胞周期和细胞凋亡。了解c-Jun法规对于制定癌症治疗策略很重要。 COP9信号体亚基6（CSN6）在泛素介导的蛋白质降解中起关键作用。 MEKK1是一个丝氨酸/苏氨酸激酶和E3连接酶，含有参与c-Jun泛素化的PHD / RING域。在这里，我们显示CSN6与MEKK1相关联，并通过促进遍在蛋白介导的MEKK1降解来降低MEKK1的表达水平。我们还表明，CSN6过表达减少了MEKK1介导的c-Jun泛素化，这在缓解渗透压介导的c-Jun下调中表现出来。因此，CSN6参与积极调节c-Jun的稳定性。 CSN6的过表达与癌症中c-Jun目标基因表达的上调相关。这些发现为CSN6-MEKK1-c-Jun轴在肿瘤发生中提供了新的见识。

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