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Roles of CREB-binding protein (CBP)/p300 in respiratory epithelium tumorigenesis

机译：CREB结合蛋白（CBP）/ p300在呼吸道上皮肿瘤发生中的作用

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CREB-binding protein (CBP) and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentiation and apoptosis. Several studies have suggested that CBP and p300 might be considered as tumour suppressors, with their prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli. They exert their actions mainly via acetylation of histones and other regulatory proteins (e.g. p53). A major paradox in CBP/ p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberrations. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimate converging point of these derangements, and CBP/p300 represents key participants in this interplay. Thus, illumination of their molecular actions and interactions could reveal new potential targets for pharmacological interventions in respiratory epithelium carcinogenesis.
机译：CREB结合蛋白（CBP）及其同源物p300是各种序列特异性转录因子的转录共激活因子，这些因子参与多种细胞活动，例如DNA修复，细胞生长，分化和凋亡。几项研究表明，CBP和p300可能被认为是肿瘤抑制因子，它们的突出作用是不同基因表达模式对各种刺激的交叉偶联。它们主要通过组蛋白和其他调节蛋白（例如p53）的乙酰化发挥作用。 CBP / p300功能的主要矛盾在于它们似乎能够促进各种相反的细胞过程。呼吸道上皮肿瘤发生代表了遗传和表观遗传畸变色域的多步累积的复杂过程。通过激活和抑制复合物交替形成的转录调控是这些失调的最终收敛点，CBP / p300代表了这种相互作用的关键参与者。因此，阐明它们的分子作用和相互作用可以揭示呼吸道上皮癌变中药理干预的新潜在靶标。

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