We are analyzing https://link.springer.com/article/10.1186/1476-4598-11-13.

Title:
Downregulation of HuR as a new mechanism of doxorubicin resistance in breast cancer cells | Molecular Cancer
Description:
Background HuR, an RNA binding protein involved in the post-transcriptional regulation of a wide spectrum of mRNAs, has been demonstrated to be a determinant of carcinogenesis and tumor aggressiveness in several cancer types. In this study, we investigated the role of HuR in the apoptosis and in the chemoresistance induced by the widely used anticancer drug doxorubicin in human breast cancer cells (MCF-7). Results We showed that HuR acts in the early phase of cell response to doxorubicin, being induced to translocate into the cytoplasm upon phosphorylation. Reducing HuR levels diminished the apoptotic response to doxorubicin. Doxorubicin-induced apoptosis was also correlated with the presence of HuR in the cytoplasm. Rottlerin, which was able to block HuR nuclear export, had correspondingly antagonistic effects with doxorubicin on cell toxicity. The proapoptotic activity of HuR was not due to cleavage to an active form, as was previously reported. In in vitro selected doxorubicin resistant MCF-7 cells (MCF-7/doxoR) overexpressing the multidrug resistance (MDR) related ABCG2 transporter, we observed a significant HuR downregulation that was paralleled by a corresponding downregulation of HuR targets and by loss of rottlerin toxicity. Restoration of HuR expression in these cells resensitized MCF-7/doxoR cells to doxorubicin, reactivating the apoptotic response. Conclusions The present study shows that HuR is necessary to elicit the apoptotic cell response to doxorubicin and that restoration of HuR expression in resistant cells resensitizes them to the action of this drug, thereby identifying HuR as a key protein in doxorubicin pharmacology.
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Keywords {🔍}

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Topics {✒️}

polysomal profile indicating pentr/sd/d-topo cloning system alessandro provenzani protein-a-coated agarose beads author information authors pt-rex-dest30 destination vector toma tebaldi author correspondence anticancer-antioxidant dual-function compound rna-binding protein elavl1/hur open access article gabriella viero luminescence-based apoptosis kit article download pdf microrna mir-548c-3p anti-h3 ab1791 abcam pan anti-phospo antibody marie-courie funding program t-test unequal variance luminescence-based viability kit pan anti-phospo antibodies antonino maria spartà = x-μ/δwere μ post-transcriptional gene regulation small-cell lung cancer rna-binding proteins tia-1 low-molecular-weight inhibitors somatic k-ras mutations anti-ldh l7016 sigma benjamini-hochberg corrected p sc-35619 santa cruz sc-29226 santa cruz sc-37007 santa cruz au-rich stability element nat rev cancer acid-washed glass coverslips rna-binding protein hur mda-mb-231 doxo-resistant cells full size image doxo-induced apoptosis activate hepes-based permeabilization buffer triple negative cells mrna-binding protein hur nuclear-cytoplasmic shuttling protein anti-hur immunoprecipitated material atp binding-cassette high-constitutive hur phosphorylation breast cancer cells translational active polyribosomes mda-mb-231/doxor cells

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         headline:Downregulation of HuR as a new mechanism of doxorubicin resistance in breast cancer cells
         description:HuR, an RNA binding protein involved in the post-transcriptional regulation of a wide spectrum of mRNAs, has been demonstrated to be a determinant of carcinogenesis and tumor aggressiveness in several cancer types. In this study, we investigated the role of HuR in the apoptosis and in the chemoresistance induced by the widely used anticancer drug doxorubicin in human breast cancer cells (MCF-7). We showed that HuR acts in the early phase of cell response to doxorubicin, being induced to translocate into the cytoplasm upon phosphorylation. Reducing HuR levels diminished the apoptotic response to doxorubicin. Doxorubicin-induced apoptosis was also correlated with the presence of HuR in the cytoplasm. Rottlerin, which was able to block HuR nuclear export, had correspondingly antagonistic effects with doxorubicin on cell toxicity. The proapoptotic activity of HuR was not due to cleavage to an active form, as was previously reported. In in vitro selected doxorubicin resistant MCF-7 cells (MCF-7/doxoR) overexpressing the multidrug resistance (MDR) related ABCG2 transporter, we observed a significant HuR downregulation that was paralleled by a corresponding downregulation of HuR targets and by loss of rottlerin toxicity. Restoration of HuR expression in these cells resensitized MCF-7/doxoR cells to doxorubicin, reactivating the apoptotic response. The present study shows that HuR is necessary to elicit the apoptotic cell response to doxorubicin and that restoration of HuR expression in resistant cells resensitizes them to the action of this drug, thereby identifying HuR as a key protein in doxorubicin pharmacology.
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      headline:Downregulation of HuR as a new mechanism of doxorubicin resistance in breast cancer cells
      description:HuR, an RNA binding protein involved in the post-transcriptional regulation of a wide spectrum of mRNAs, has been demonstrated to be a determinant of carcinogenesis and tumor aggressiveness in several cancer types. In this study, we investigated the role of HuR in the apoptosis and in the chemoresistance induced by the widely used anticancer drug doxorubicin in human breast cancer cells (MCF-7). We showed that HuR acts in the early phase of cell response to doxorubicin, being induced to translocate into the cytoplasm upon phosphorylation. Reducing HuR levels diminished the apoptotic response to doxorubicin. Doxorubicin-induced apoptosis was also correlated with the presence of HuR in the cytoplasm. Rottlerin, which was able to block HuR nuclear export, had correspondingly antagonistic effects with doxorubicin on cell toxicity. The proapoptotic activity of HuR was not due to cleavage to an active form, as was previously reported. In in vitro selected doxorubicin resistant MCF-7 cells (MCF-7/doxoR) overexpressing the multidrug resistance (MDR) related ABCG2 transporter, we observed a significant HuR downregulation that was paralleled by a corresponding downregulation of HuR targets and by loss of rottlerin toxicity. Restoration of HuR expression in these cells resensitized MCF-7/doxoR cells to doxorubicin, reactivating the apoptotic response. The present study shows that HuR is necessary to elicit the apoptotic cell response to doxorubicin and that restoration of HuR expression in resistant cells resensitizes them to the action of this drug, thereby identifying HuR as a key protein in doxorubicin pharmacology.
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         Doxorubicin
         Drug resistance
         Apoptosis
         Translational regulation
         Cancer Research
         Oncology
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      name:Laboratory of Translational Genomics, Centre for Integrative Biology, CIBIO, University of Trento, Trento, Italy
      name:Laboratory of Genomic Screening, Centre for Integrative Biology, CIBIO, University of Trento, Trento, Italy

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