We are analyzing https://link.springer.com/article/10.1007/s10549-007-9751-0.

Title:
Trichostatin A and 5 Aza-2′ deoxycytidine decrease estrogen receptor mRNA stability in ER positive MCF7 cells through modulation of HuR | Breast Cancer Research and Treatment
Description:
Trichostatin A (TSA) and 5-Aza 2′deoxycytidine (AZA), two well characterized pharmacologic inhibitors of histone deacetylation and DNA methylation, affect estrogen receptor alpha (ER) levels differently in ER-positive versus ER-negative breast cancer cell lines. Whereas pharmacologic inhibition of these epigenetic mechanisms results in re-expression and increased estrogen receptor alpha (ER) levels in ER-negative cells, treatment in ER-positive MCF7 cells results in decreased ER mRNA and protein levels. This decrease is dependent upon protein interaction with the ER 3′UTR. Actinomycin D studies showed a 37.5% reduction in ER mRNA stability from 4 to 1.5 h in AZA/TSA treated MCF7 cell lines; an effect not seen in 231ER + cells transfected with the ER coding region but lacking incorporation of the 3′UTR. AZA/TSA do not appear to directly interact with the 3′UTR but rather decrease stability through altered subcellular localization of the RNA binding protein, HuR. siRNA inhibition of HuR expression reduces both the steady-state and stability of ER mRNA, suggesting that HuR plays a critical role in the control of ER mRNA stability. Our data suggest that epigenetic modulators can alter stability through modulation of HuR subcellular distribution. Taken together, these data provide a novel anti-estrogenic mechanism for AZA and TSA in ER positive human breast cancer cells.
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Keywords {🔍}

cancer, estrogen, article, receptor, google, scholar, breast, cas, pubmed, cells, res, hur, mrna, alpha, human, stability, expression, histone, protein, aza, keen, deacetylase, trichostatin, mcf, gene, privacy, cookies, content, data, research, deoxycytidine, methylation, levels, cell, inhibition, utr, region, rna, access, tamoxifen, clin, biol, publish, search, treatment, decrease, modulation, proteins, untranslated, treat,

Topics {✒️}

month download article/chapter 5-aza-2′-deoxycytidine-induced cytotoxicity estrogen-independent aggressive phenotype estrogen receptor gene estrogen receptor alpha adenine/uridine-rich elements judith clancy keen related subjects er-negative cells rna-binding proteins human breast cancer nuclear-cytoplasmic shuttling protein human breast carcinoma breast cancer cells functional estrogen receptor promotes proteasomal degradation estrogen receptor expression protein phosphatase 2a rna binding protein full article pdf breast cancer patients resistant breast cancer er mrna stability overcoming endocrine resistance hur expression reduces privacy choices/manage cookies 231er + cells transfected decreased er mrna keen jc estrogen receptor estrogen receptor ∝ identifying mrna subsets histone deacetylase inhibitor ectopic hormone er steroid hormone receptors cancer cell 10 epigenetic mechanisms results breast cancer article pryzbylkowski er coding region european economic area altered subcellular localization anti-estrogenic mechanism chronic oxidative stress nass sj higher tumor grade cytoplasmic hur expression increased cyclooxygenase-2 expression histone deacetylase inhibition conditions privacy policy

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         description:Trichostatin A (TSA) and 5-Aza 2′deoxycytidine (AZA), two well characterized pharmacologic inhibitors of histone deacetylation and DNA methylation, affect estrogen receptor alpha (ER) levels differently in ER-positive versus ER-negative breast cancer cell lines. Whereas pharmacologic inhibition of these epigenetic mechanisms results in re-expression and increased estrogen receptor alpha (ER) levels in ER-negative cells, treatment in ER-positive MCF7 cells results in decreased ER mRNA and protein levels. This decrease is dependent upon protein interaction with the ER 3′UTR. Actinomycin D studies showed a 37.5% reduction in ER mRNA stability from 4 to 1.5 h in AZA/TSA treated MCF7 cell lines; an effect not seen in 231ER + cells transfected with the ER coding region but lacking incorporation of the 3′UTR. AZA/TSA do not appear to directly interact with the 3′UTR but rather decrease stability through altered subcellular localization of the RNA binding protein, HuR. siRNA inhibition of HuR expression reduces both the steady-state and stability of ER mRNA, suggesting that HuR plays a critical role in the control of ER mRNA stability. Our data suggest that epigenetic modulators can alter stability through modulation of HuR subcellular distribution. Taken together, these data provide a novel anti-estrogenic mechanism for AZA and TSA in ER positive human breast cancer cells.
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      description:Trichostatin A (TSA) and 5-Aza 2′deoxycytidine (AZA), two well characterized pharmacologic inhibitors of histone deacetylation and DNA methylation, affect estrogen receptor alpha (ER) levels differently in ER-positive versus ER-negative breast cancer cell lines. Whereas pharmacologic inhibition of these epigenetic mechanisms results in re-expression and increased estrogen receptor alpha (ER) levels in ER-negative cells, treatment in ER-positive MCF7 cells results in decreased ER mRNA and protein levels. This decrease is dependent upon protein interaction with the ER 3′UTR. Actinomycin D studies showed a 37.5% reduction in ER mRNA stability from 4 to 1.5 h in AZA/TSA treated MCF7 cell lines; an effect not seen in 231ER + cells transfected with the ER coding region but lacking incorporation of the 3′UTR. AZA/TSA do not appear to directly interact with the 3′UTR but rather decrease stability through altered subcellular localization of the RNA binding protein, HuR. siRNA inhibition of HuR expression reduces both the steady-state and stability of ER mRNA, suggesting that HuR plays a critical role in the control of ER mRNA stability. Our data suggest that epigenetic modulators can alter stability through modulation of HuR subcellular distribution. Taken together, these data provide a novel anti-estrogenic mechanism for AZA and TSA in ER positive human breast cancer cells.
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