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首页> 外文期刊>Journal of Cellular Physiology >p53 Suppresses lung resistance-related protein expression through Y-box binding protein 1 in the MCF-7 breast tumor cell line.
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p53 Suppresses lung resistance-related protein expression through Y-box binding protein 1 in the MCF-7 breast tumor cell line.

机译：p53抑制肺resistance-related蛋白质通过Y-box结合蛋白1表达MCF-7乳房肿瘤细胞系。

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Lung resistance-related protein (LRP) has roles in multi-drug resistance of tumor cells. Understanding the mechanisms that regulate LRP expression in tumor cells is an important research area. A putative p53 response element in the LRP promoter has been found. Thus, p53-related regulation of LRP expression was explored in this study. We first demonstrated that p53 overexpression inhibited LRP expression both at the protein and mRNA levels. Then, using a dual-luciferase reporter assay, we located the p53 response element to the Y-box (-263~-407) of the LRP promoter, the YB-1 binding site, but not the putative p53 response element. Furthermore, coimmunoprecipitation and chromatin immunoprecipitation showed p53 could bind to the Y-box of the LRP promoter through interaction of p53 with YB-1. YB-1 coexpression with p53 facilitated p53-induced suppression of endogenous LRP expression in MCF-7 cells. HDAC2, a corepressor of p53, was found to also interact with YB-1, and this interaction was mediated by p53. These results showed that the p53-HDAC2 transcriptional repressor complex can bind to the Y-box of the LRP promoter and repress LRP expression through interaction with YB-1. p53-related suppression of LRP expression was completely reversed by doxorubicin treatment and Adr, whereas CP and VP-16 treatment induced LRP expression increased significantly. Inhibition of LRP expression by siRNA facilitated Adr induced apoptosis of MCF-7 cells. All these findings indicated that loss of p53-related suppression of LRP may be the reason for LRP expression increase, and, therefore, chemotherapy resistance in tumor cells.
机译：肺resistance-related蛋白质(单体)的角色肿瘤细胞的多药耐药性。理解的机制调节单体表达在肿瘤细胞是重要的研究领域。含启动子被发现。p53-related单体表达的调节探讨了在这个研究。, p53过度抑制含表达式蛋白质和mRNA水平。dual-luciferase记者分析,我们找到了p53响应元素Y-box (-263 ~ -407)含启动子,YB-1结合位点,但不是假定的p53响应元素。coimmunoprecipitation和染色质免疫沉淀反应显示p53能绑定到的通过互动Y-box含碘的启动子p53 YB-1。促进p53诱导内源性抑制单体在MCF-7细胞表达。p53的辅阻遏物,被发现也相互作用YB-1,这种互动是由p53。可以绑定到转录抑制因子复杂Y-box含启动子和镇压部队通过与YB-1表达式。p53-related抑制含表达式阿霉素治疗和完全逆转美国存托凭证,而CP和VP-16治疗诱导单体表达显著增加。含碘siRNA促进Adr诱导表达MCF-7细胞的凋亡。表明p53-related镇压的损失含含表达可能是原因增加,因此,化疗抵抗在肿瘤细胞。

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