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首页> 外文期刊>Molecular and Cellular Biology >Protein Kinase Cζ Represses the Interleukin-6 Promoter and Impairs Tumorigenesis In Vivo
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Protein Kinase Cζ Represses the Interleukin-6 Promoter and Impairs Tumorigenesis In Vivo

机译：蛋白激酶Cζ抑制白介素6启动子并损害体内肿瘤发生。

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摘要

Gene alterations in tumor cells that confer the ability to grow under nutrient- and mitogen-deficient conditions constitute a competitive advantage that leads to more-aggressive forms of cancer. The atypical protein kinase C (PKC) isoform, PKCζ, has been shown to interact with the signaling adapter p62, which is important for Ras-induced lung carcinogenesis. Here we show that PKCζ-deficient mice display increased Ras-induced lung carcinogenesis, suggesting a new role for this kinase as a tumor suppressor in vivo. We also show that Ras-transformed PKCζ-deficient lungs and embryo fibroblasts produced more interleukin-6 (IL-6), which we demonstrate here plays an essential role in the ability of Ras-transformed cells to grow under nutrient-deprived conditions in vitro and in a mouse xenograft system in vivo. We also show that PKCζ represses histone acetylation at the C/EBPβ element in the IL-6 promoter. Therefore, PKCζ, by controlling the production of IL-6, is a critical signaling molecule in tumorigenesis.
机译：赋予癌细胞在营养缺乏和促分裂原缺乏条件下生长的能力的肿瘤细胞中的基因改变，构成了竞争优势，导致更具侵略性的癌症。非典型蛋白激酶C（PKC）亚型PKCζ已显示与信号转导子p62相互作用，这对Ras诱导的肺癌发生很重要。在这里，我们显示PKCζ缺陷小鼠显示增加的Ras诱导的肺癌发生，表明该激酶作为体内肿瘤抑制因子的新作用。我们还显示了Ras转化的PKCζ缺陷型肺和胚胎成纤维细胞产生了更多的白介素6（IL-6），我们在此证明了Ras转化的细胞在营养缺乏条件下体外生长的能力中起着至关重要的作用。在体内的小鼠异种移植系统中。我们还显示，PKCζ抑制IL-6启动子中C /EBPβ元件处的组蛋白乙酰化。因此，通过控制IL-6的产生，PKCζ是肿瘤发生中的关键信号分子。

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