We are analyzing https://link.springer.com/article/10.1186/1471-2407-14-498.

Title:
The aryl hydrocarbon receptor ligand omeprazole inhibits breast cancer cell invasion and metastasis | BMC Cancer
Description:
Background Patients with ER-negative breast tumors are among the most difficult to treat and exhibit low survival rates due, in part, to metastasis from the breast to various distal sites. Aryl hydrocarbon receptor (AHR) ligands show promise as antimetastatic drugs for estrogen receptor (ER)-negative breast cancer. Methods Triple negative MDA-MB-231 breast cancer cells were treated with eight AHR-active pharmaceuticals including 4-hydroxtamoxifen, flutamide leflunomide, mexiletine, nimodipine, omeprazole, sulindac and tranilast, and the effects of these compounds on cell proliferation (MTT assay) and cell migration (Boyden chamber assay) were examined. The role of the AHR in mediating inhibition of MDA-MB-231 cell invasion was investigated by RNA interference (RNAi) and knockdown of AHR or cotreatment with AHR agonists. Lung metastasis of MDA-MB-231 cells was evaluated in mice administered cells by tail vein injection and prometastatic gene expression was examined by immunohistochemistry. Results We showed that only the proton pump inhibitor omeprazole decreased MDA-MB-231 breast cancer cell invasion in vitro. Omeprazole also significantly decreased MDA-MB-231 cancer cell metastasis to the lung in a mouse model (tail vein injection), and in vitro studies showed that omeprazole decreased expression of at least two prometastatic genes, namely matrix metalloproteinase-9 (MMP-9) and C-X-C chemokine receptor 4 (CXCR4). Results of RNA interference studies confirmed that omeprazole-mediated downregulation of CXCR4 (but not MMP-9) was AHR-dependent. Chromatin immunoprecipitation assays demonstrated that omeprazole recruited the AHR to regions in the CXCR4 promoter that contain dioxin response elements (DREs) and this was accompanied by the loss of pol II on the promoter and decreased expression of CXCR4. Conclusions AHR-active pharmaceuticals such as omeprazole that decrease breast cancer cell invasion and metastasis may have important clinical applications for late stage breast cancer chemotherapy.
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Keywords {🔍}

cells, omeprazole, ahr, mdamb, cancer, cxcr, cell, figure, pubmed, receptor, breast, article, google, scholar, invasion, cas, tcdd, aryl, hydrocarbon, treated, activity, cypa, metastasis, expression, decreased, effects, pharmaceuticals, results, ahractive, assay, mrna, methods, inhibition, mmp, promoter, observed, determined, safe, studies, outlined, role, dmso, file, induction, inhibited, levels, dre, migration, binding, transfected,

Topics {✒️}

triple-negative mda-mb-231 cells er-negative mda-mb-468 cells 8-tetrachlorodibenzo-p-dioxin-induced porphyria 8-tetrachlorodibenzo-p-dioxin-responsive promoters mda-mb-468 cell lines 8-tetrachlorodibenzo-p-dioxin-mediated induction ligand-activated transcription factor mda-mb-231 cell invasion open access license ligand-mediated selective modulation female sprague-dawley rats pre-publication history ahr antagonist 3′4′-dimethoxy-α-naphthoflavone er-negative breast tumors polychlorinated dibenzo-p-dioxins proton pump inhibitor exhibits anti-inflammatory properties negative breast cancer 8-tetrachlorodibenzo-p-dioxin antagonist 8- tetrachlorodibenzo-p-dioxin antagonist mda-mb-231 cells paralleled cell context-dependent variability observe ligand-dependent recruitment article download pdf stem cell stability dmba-induced mammary tumors inhibited tcdd-induced toxicity bd-matrigel invasion chamber mda-mb-231 cells cotreated aryl hydrocarbon receptor mda-mb-231 cells transfected full size image inhibitory ahr-estrogen receptor ahr-active pharmaceuticals including 8-tetrachlorodibenzo-p-dioxin antagonists proton pump inhibitors proximal ah-responsive region cancer cell invasion breast cancer cells aryl hydrocarbon hydroxylase pure aryl hydrocarbon murine breast cancer t1 breast cancer potential anti-inflammatory effects treatment-related weight loss syng-ook lee breast cancer metastasis antimetastatic pathway ahr-active antimetastatic agent pro-metastatic gene cxcr4

Questions {❓}

Miyashita T, Shah FA, Harmon JW, Marti GP, Matsui D, Okamoto K, Makino I, Hayashi H, Oyama K, Nakagawara H, Tajima H, Fujita H, Takamura H, Murakami M, Ninomiya I, Kitagawa H, Fushida S, Fujimura T, Ohta T: Do proton pump inhibitors protect against cancer progression in GERD?

Schema {🗺️}

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         headline:The aryl hydrocarbon receptor ligand omeprazole inhibits breast cancer cell invasion and metastasis
         description:Patients with ER-negative breast tumors are among the most difficult to treat and exhibit low survival rates due, in part, to metastasis from the breast to various distal sites. Aryl hydrocarbon receptor (AHR) ligands show promise as antimetastatic drugs for estrogen receptor (ER)-negative breast cancer. Triple negative MDA-MB-231 breast cancer cells were treated with eight AHR-active pharmaceuticals including 4-hydroxtamoxifen, flutamide leflunomide, mexiletine, nimodipine, omeprazole, sulindac and tranilast, and the effects of these compounds on cell proliferation (MTT assay) and cell migration (Boyden chamber assay) were examined. The role of the AHR in mediating inhibition of MDA-MB-231 cell invasion was investigated by RNA interference (RNAi) and knockdown of AHR or cotreatment with AHR agonists. Lung metastasis of MDA-MB-231 cells was evaluated in mice administered cells by tail vein injection and prometastatic gene expression was examined by immunohistochemistry. We showed that only the proton pump inhibitor omeprazole decreased MDA-MB-231 breast cancer cell invasion in vitro. Omeprazole also significantly decreased MDA-MB-231 cancer cell metastasis to the lung in a mouse model (tail vein injection), and in vitro studies showed that omeprazole decreased expression of at least two prometastatic genes, namely matrix metalloproteinase-9 (MMP-9) and C-X-C chemokine receptor 4 (CXCR4). Results of RNA interference studies confirmed that omeprazole-mediated downregulation of CXCR4 (but not MMP-9) was AHR-dependent. Chromatin immunoprecipitation assays demonstrated that omeprazole recruited the AHR to regions in the CXCR4 promoter that contain dioxin response elements (DREs) and this was accompanied by the loss of pol II on the promoter and decreased expression of CXCR4. AHR-active pharmaceuticals such as omeprazole that decrease breast cancer cell invasion and metastasis may have important clinical applications for late stage breast cancer chemotherapy.
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            Metastasis
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            Cancer Research
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      headline:The aryl hydrocarbon receptor ligand omeprazole inhibits breast cancer cell invasion and metastasis
      description:Patients with ER-negative breast tumors are among the most difficult to treat and exhibit low survival rates due, in part, to metastasis from the breast to various distal sites. Aryl hydrocarbon receptor (AHR) ligands show promise as antimetastatic drugs for estrogen receptor (ER)-negative breast cancer. Triple negative MDA-MB-231 breast cancer cells were treated with eight AHR-active pharmaceuticals including 4-hydroxtamoxifen, flutamide leflunomide, mexiletine, nimodipine, omeprazole, sulindac and tranilast, and the effects of these compounds on cell proliferation (MTT assay) and cell migration (Boyden chamber assay) were examined. The role of the AHR in mediating inhibition of MDA-MB-231 cell invasion was investigated by RNA interference (RNAi) and knockdown of AHR or cotreatment with AHR agonists. Lung metastasis of MDA-MB-231 cells was evaluated in mice administered cells by tail vein injection and prometastatic gene expression was examined by immunohistochemistry. We showed that only the proton pump inhibitor omeprazole decreased MDA-MB-231 breast cancer cell invasion in vitro. Omeprazole also significantly decreased MDA-MB-231 cancer cell metastasis to the lung in a mouse model (tail vein injection), and in vitro studies showed that omeprazole decreased expression of at least two prometastatic genes, namely matrix metalloproteinase-9 (MMP-9) and C-X-C chemokine receptor 4 (CXCR4). Results of RNA interference studies confirmed that omeprazole-mediated downregulation of CXCR4 (but not MMP-9) was AHR-dependent. Chromatin immunoprecipitation assays demonstrated that omeprazole recruited the AHR to regions in the CXCR4 promoter that contain dioxin response elements (DREs) and this was accompanied by the loss of pol II on the promoter and decreased expression of CXCR4. AHR-active pharmaceuticals such as omeprazole that decrease breast cancer cell invasion and metastasis may have important clinical applications for late stage breast cancer chemotherapy.
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         Ah receptor
         Metastasis
         Inhibition
         CXCR4
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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      affiliation:
            name:Texas A&M Health Sciences Center
            address:
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               type:PostalAddress
            type:Organization
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      affiliation:
            name:Texas A&M University
            address:
               name:Department of Veterinary Pathobiology, Texas A&M University, College Station, USA
               type:PostalAddress
            type:Organization
      name:Stephen Safe
      affiliation:
            name:Texas A&M Health Sciences Center
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      name:Department of Veterinary Pathobiology, Texas A&M University, College Station, USA
      name:Institute of Biosciences and Technology, Texas A&M Health Sciences Center, Houston, USA
      name:Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, USA

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