We are analyzing https://link.springer.com/article/10.1007/s10549-010-1240-1.

Title:
Nuclear co-localization and functional interaction of COX-2 and HIF-1α characterize bone metastasis of human breast carcinoma | Breast Cancer Research and Treatment
Description:
The aim of this article is to identify nuclear co-localization of COX-2 and HIF-1α in human-bone metastasis of breast cancer, index of transcriptionally activated cells and functional for gene expression. In particular, we verified whether hypoxia exerted a direct role on metastasis-gene expression or through COX-2 signaling, due to the relevance for clinical implications to individuate molecular targets for diagnosis and therapy. The experiments were performed in vitro with two metastatic clones, 1833 and MDA-231BO, and the parental MDA-MB231 cells, in vivo (1833-xenograft model), and in human-bone metastasis specimens. In 1833 cells in vitro, COX-2 signaling pathway was critical for nuclear HIF-1α-protein expression/translocation, mechanisms determining HIF-1 activity and gene expression. The data were corroborated by immunohistochemistry in human-bone metastasis specimens. COX-2 and HIF-1α showed wide co-localization in the nucleus, indicative of COX-2-nuclear import in transcriptionally activated metastatic cells and consistent with COX-2-HIF-1α functional interaction. A network of microenvironmental signals controlled COX-2 induction and HIF-1 activation downstream. In fact, hypoxia through HGF and TGF-β1 autoregulatory loops triggered a specific array of transcription factors responsible for COX-2 transactivation. The novelty was that HGF and TGF-β1 biological signals were produced by hypoxic metastatic cells and, therefore, the microenvironment seemed to be modified by metastatic-cell engraftment in the bone. In agreement, HIF-1α expression in bone marrow supportive cells occurred in metastasis-bearing animals. Altogether, the data supported the pre-metastatic-niche theory. Our observations might be useful to design therapies against bone metastasis, by affecting the phenotype changes of metastatic cells occurring at the secondary growth site through COX-2-HIF-1 interaction.
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article, cancer, google, scholar, cas, pubmed, breast, metastasis, bone, cells, cell, cox, expression, hypoxia, growth, res, nuclear, matteucci, desiderio, factor, hif, human, carcinoma, maroni, access, tumor, mol, hifα, metastatic, activity, rev, privacy, cookies, content, data, research, interaction, paola, bendinelli, role, signaling, microenvironment, metastases, hepatocyte, physiol, treat, information, publish, search, colocalization,

Topics {✒️}

hypoxia-inducible factor-1alpha correlates stromal cell-derived factor-1α nuclear hif-1α-protein expression/translocation month download article/chapter hypoxia-inducible factor 1α parental mda-mb231 cells tgf-β1 biological signals node-negative breast cancer human-bone metastasis specimens hepatocyte growth factor von hippel-lindau loss hypoxia-inducible factors hif-1α showed wide β-catenin/wnt pathways maria alfonsina desiderio cox-2-hif-1α functional interaction human-breast cancer metastasis lymph node metastases transcription factors responsible pre-metastatic-niche theory ministero istruzione-università-ricerca tgf-β signaling secondary growth site related subjects human breast carcinoma human-bone metastasis primary tumor growth full article pdf nf-kb activation context-dependent transcriptional regulation human bone discs tumor-stromal interactions breast cancer metastasis privacy choices/manage cookies stilbene-induced cox-2 transcriptionally activated cells hif-1 activation downstream variant arnt protein parallel signaling pathways hif-1α expression breast cancer tissue function induces expression primary breast cancers giuseppe perrucchini hypoxic metastatic cells metastatic cells occurring common human cancers metastasis-bearing animals metastatic-cell engraftment check access

Questions {❓}

Marignol L, Coffey M, Lawler M, Hollywood D (2008) Hypoxia in prostate cancer: a powerful shield against tumour destruction?

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      description:The aim of this article is to identify nuclear co-localization of COX-2 and HIF-1α in human-bone metastasis of breast cancer, index of transcriptionally activated cells and functional for gene expression. In particular, we verified whether hypoxia exerted a direct role on metastasis-gene expression or through COX-2 signaling, due to the relevance for clinical implications to individuate molecular targets for diagnosis and therapy. The experiments were performed in vitro with two metastatic clones, 1833 and MDA-231BO, and the parental MDA-MB231 cells, in vivo (1833-xenograft model), and in human-bone metastasis specimens. In 1833 cells in vitro, COX-2 signaling pathway was critical for nuclear HIF-1α-protein expression/translocation, mechanisms determining HIF-1 activity and gene expression. The data were corroborated by immunohistochemistry in human-bone metastasis specimens. COX-2 and HIF-1α showed wide co-localization in the nucleus, indicative of COX-2-nuclear import in transcriptionally activated metastatic cells and consistent with COX-2-HIF-1α functional interaction. A network of microenvironmental signals controlled COX-2 induction and HIF-1 activation downstream. In fact, hypoxia through HGF and TGF-β1 autoregulatory loops triggered a specific array of transcription factors responsible for COX-2 transactivation. The novelty was that HGF and TGF-β1 biological signals were produced by hypoxic metastatic cells and, therefore, the microenvironment seemed to be modified by metastatic-cell engraftment in the bone. In agreement, HIF-1α expression in bone marrow supportive cells occurred in metastasis-bearing animals. Altogether, the data supported the pre-metastatic-niche theory. Our observations might be useful to design therapies against bone metastasis, by affecting the phenotype changes of metastatic cells occurring at the secondary growth site through COX-2-HIF-1 interaction.
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