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首页> 外文期刊>Breast cancer research and treatment. >The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines.
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The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines.

机译：RNA结合蛋白HuR调节人乳腺癌细胞系中GATA3 mRNA的稳定性。

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Meta-analyses of microarray data indicate that GATA3 is co-expressed with estrogen receptor alpha (ER) in breast cancer cells. While the significance of this remains unclear, it is thought that GATA3 may serve as a prognostic indicator in breast tumors and may play a role in ER signaling. Recently, reciprocal regulation of GATA3 and ER transcription was demonstrated, suggesting that control of their expression is intertwined. We sought to determine whether GATA3 and ER expression was also coordinately regulated at other levels. Unlike ER, GATA3 was not under epigenetic control and was not re-expressed in the presence of DNMT or HDAC inhibitors in ER/GATA3-negative cells. However, like ER, these inhibitors decreased GATA3 expression in ER/GATA3-positive cell lines. We have previously reported that ER mRNA stability is increased through binding of the RNA-binding protein HuR/ELAV1 to the 3'untranslated region (UTR) and that DNMT and HDAC inhibitors reduce ER expression by altering this interaction. Biotin pull-down assays using a biotinylated GATA3 RNA probe confirmed that HuR also binds to the GATA3 3'UTR. Inhibition of HuR using siRNA probes decreased GATA3 mRNA, mRNA stability and protein expression, indicating that HuR plays a role in regulating GATA3 expression. Inhibition of either HuR or GATA3 reduced cell growth of MCF7 cells. Based on our findings, it is clear that coordinate regulation of ER and GATA3 occurs, however differences do exist. These findings may aid in identification of new targets that control cell growth of breast cancer cells.
机译：基因芯片数据的荟萃分析表明，GATA3与乳腺癌细胞中的雌激素受体α（ER）共表达。尽管其重要性尚不清楚，但人们认为GATA3可以作为乳腺肿瘤的预后指标，并可能在ER信号传导中发挥作用。最近，证明了相互调节GATA3和ER转录，表明对它们表达的控制相互交织。我们试图确定GATA3和ER表达是否在其他水平上也受到协调调控。与ER不同，GATA3不在表观遗传控制下，在DNMT或HDAC抑制剂存在的情况下，ER / GATA3阴性细胞中也不会重新表达。但是，与ER一样，这些抑制剂会降低ER / GATA3阳性细胞系中GATA3的表达。我们以前曾报道过，通过将RNA结合蛋白HuR / ELAV1与3'非翻译区（UTR）结合，ER的mRNA稳定性得以提高，并且DNMT和HDAC抑制剂通过改变这种相互作用而降低了ER的表达。使用生物素化的GATA3 RNA探针进行的生物素下拉试验证实，HuR也与GATA3 3'UTR结合。使用siRNA探针抑制HuR会降低GATA3 mRNA，mRNA稳定性和蛋白质表达，表明HuR在调节GATA3表达中起作用。抑制HuR或GATA3会降低MCF7细胞的细胞生长。根据我们的发现，很明显，ER和GATA3发生了协调调节，但是确实存在差异。这些发现可能有助于识别控制乳腺癌细胞生长的新靶标。

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