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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Inhibition of p53-induced apoptosis without affecting expression of p53-regulated genes
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Inhibition of p53-induced apoptosis without affecting expression of p53-regulated genes

机译：抑制p53诱导的细胞凋亡而不影响p53调控基因的表达

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摘要

Using DNA microarray and clustering of expressed genes we have analyzed the mechanism of inhibition of wild-type p53-induced apoptosis by the cytokine interleukin 6 (IL-6) and the calcium mobilizer thapsigargin (TG). Clustering analysis of 1,786 genes, the expression level of which changed after activation of wild-type p53 in the absence or presence of IL-6 or TG, showed that these compounds did not cause a general inhibition of the ability of p53 to up-regulate or down-regulate gene expression. Expression of various p53 targets implicated as mediators of p53-induced apoptosis was also not affected by IL-6 or TG. These compounds thus can bypass the effect of wild-type p53 on gene expression and inhibit apoptosis. IL-6 and TG activated different p53-independent pathways of gene expression that include up-regulation of antiapoptotic genes. IL-6 and TG also activated different differentiation-associated genes. The ability of compounds such as cytokines and calcium mobilizers to inhibit p53-mediated apoptosis without generally inhibiting gene expression regulated by p53 can facilitate tumor development and tumor resistance to radiation and chemotherapy in cells that retain wild-type p53. [References: 40]
机译：我们使用DNA芯片和表达基因的聚类分析了细胞因子白介素6（IL-6）和钙动员毒胡萝卜素（TG）抑制野生型p53诱导的细胞凋亡的机制。对1,786个基因的聚类分析，其表达水平在不存在或存在IL-6或TG的情况下激活了野生型p53后发生了改变，表明这些化合物并未普遍抑制p53上调的能力或下调基因表达。 IL-6或TG不影响与p53诱导的细胞凋亡有关的各种p53靶标的表达。因此，这些化合物可以绕过野生型p53对基因表达的作用并抑制细胞凋亡。 IL-6和TG激活了基因表达的不同p53独立途径，其中包括抗凋亡基因的上调。 IL-6和TG也激活了不同的分化相关基因。化合物（例如细胞因子和钙动员剂）抑制p53介导的细胞凋亡而通常不抑制p53调节的基因表达的能力可以促进保留野生型p53的细胞的肿瘤发展以及对放射线和化疗的耐药性。 [参考：40]

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