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We began analyzing https://link.springer.com/article/10.1007/s10549-009-0517-8, but it redirected us to https://link.springer.com/article/10.1007/s10549-009-0517-8. The analysis below is for the second page.

Title[redir]:
The RNA-binding protein HuR regulates GATA3 mRNA stability in human breast cancer cell lines | Breast Cancer Research and Treatment
Description:
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.

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Keywords {🔍}

cancer, article, breast, google, scholar, pubmed, cas, gata, estrogen, receptor, expression, cells, human, cell, res, hur, mrna, gene, davidson, keen, biol, alpha, access, protein, stability, licata, mol, privacy, cookies, content, research, rnabinding, lines, hostetter, rna, inhibition, tamoxifen, proteins, histone, deacetylase, data, information, publish, search, lauren, dnmt, binding, untranslated, region, open,

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prb2/p130–e2f4/5-hdac1-suv39h1–p300 rna-binding protein hur/elav1 er/gata3-positive cell lines month download article/chapter human estrogen receptor-{alpha} 5-aza 2â€²-deoxycytidine 5-aza-2′-deoxycytidine-induced cytotoxicity er/gata3-negative cells micro-ribonucleic acid er mrna stability judith clancy keen estrogen receptor gene multiple high-throughput analyses prb family proteins related subjects estrogen receptor alpha estrogen receptor-{alpha} estrogen receptor α human breast tumors mrna stability functional estrogen receptor breast cancer cells gene expression profiling interleukin-4 gene expression full article pdf privacy choices/manage cookies androgen receptor interacts luminal cell fate keen jc primary breast carcinomas hu proteins luminal-cell differentiation mcf7 cells hepatocellular carcinoma cells control cell growth regulating gata3 expression estrogen receptor annexin a1 expression european economic area van der wees mouse strain susceptibility antisense oligonucleotides induces diverse molecular functions check access instant access conditions privacy policy reciprocal regulation coordinate regulation histone deacetylase inhibitor breast cancer

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