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p53- and Mdm2-Independent Repression of NF-kB Transactivation by the ARF Tumor suppressor

机译：ARF肿瘤抑制因子对p53和Mdm2的NF-kB反式激活的抑制

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摘要

One mechanism by which a cell affords protection from the transforming effects of oncogenes is via the action of the tumor suppressor, ARF, which activates p53 by inactivating Mdm2. Many oncogenes have also been shown to activate the transcription factor NF-kB, which can contribute toward the malignant phenotype in many ways, including an ability to antagonize p53. Here we find that ARF inhibits NF-kB function and its antiapoptotic activity independent of Mdm2 and p53. ARF represses the transcriptional activation domain of the NF-kB family member RelA by inducing its association with the histone deacetylase, HDAC1. Further, we show that the response of NF-kb to the oncogene Bcr-Abl is determined by the ARF status of the cell. These results reveal an important function of ARF that can regulate the NF-kB response to oncogene activation.
机译：细胞提供保护免受癌基因转化作用的一种机制是通过肿瘤抑制因子ARF的作用，该因子通过失活Mdm2激活p53。还显示出许多致癌基因可激活转录因子NF-kB，该因子可通过多种方式促进恶性表型，包括拮抗p53的能力。在这里，我们发现ARF抑制NF-kB功能及其抗凋亡活性，独立于Mdm2和p53。 ARF通过诱导其与组蛋白脱乙酰基酶HDAC1的结合来抑制NF-kB家族成员RelA的转录激活结构域。此外，我们表明NF-kb对癌基因Bcr-Abl的反应是由细胞的ARF状态决定的。这些结果揭示了ARF的重要功能，它可以调节NF-kB对癌基因激活的反应。

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