Girgert, Rainer

[["dc.bibliographiccitation.firstpage","440"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","NEUROENDOCRINOLOGY LETTERS"],["dc.bibliographiccitation.lastpage","444"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Bartsch, C."],["dc.contributor.author","Hill, S. M."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:34:30Z"],["dc.date.available","2018-11-07T10:34:30Z"],["dc.date.issued","2003"],["dc.description.abstract","OBJECTIVES: Detection of the antiestrogenic effect of melatonin on various breast cancer cell lines and its dependence of the differential expression of estrogen receptors (ERalpha and ERbeta) and melatonin receptors (mt1 and RZRalpha,). SETTING AND DESIGN: Dose-response curves of estradiol were determined in 6 different breast cancer cell lines using a colorimetric proliferation assay in the absence or presence of various melatonin concentrations. METHODS: In order to detect the minor growth inhibitory effect of melatonin, a simple yet novel approach was employed: instead of incubating cells at single estradiol-concentrations at increasing melatonin levels, breast cancer cells were grown in microwell-plates for 4 days at increasing concentrations of estradiol (10(-12) M - 10(-10) M) in the absence or presence of melatonin (10(-9) M - 10(-8) M). Cell number was determined using Alamar blue and colorimetry, RT-PCR was performed for the expression of ERalpha, ERbeta, RZRalpha and mt1. RESULTS: Melatonin at concentrations of 10(-9) M and 5x10(-9) M shifted the dose-response curves of estradiol to higher concentrations. Responsiveness to melatonin depended on expression of ERalpha but not on ERbeta. mRNA of ERbeta was not detectable in the breast cancer cell lines used. Only small amounts of mt1 transcripts were detectable in MCF-7 cells of one source. In MCF-7 cells transfected with the mt1 gene and in an ovarian cancer cell line mt1 was expressed at significant levels. RZRalpha was expressed in all tested cell lines at different amounts. CONCLUSION: The growth of all ERalpha-positive breast cancer cell lines can be inhibited by melatonin. The effect in most cell lines is weak yet clearly reproducible. RZRalpha clearly contributes to the growth inhibitory effect of melatonin."],["dc.identifier.isi","000187882100012"],["dc.identifier.pmid","15073572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44887"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Maghira & Maas Publications"],["dc.relation.issn","0172-780X"],["dc.title","Tracking, the elusive antiestrogenic effect of melatonin: A new methodological approach"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","334"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Gynecological Cancer"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:31:09Z"],["dc.date.available","2018-11-07T08:31:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Effects of electromagnetic fields (EMFs) on the incidence of breast cancer (BC) have been proposed by a number of epidemiological studies. The molecular mechanism of the impact of EMFs on cells is not yet clear, although changes in gene expression have been reported in various cellular systems. In this investigation, the interference of low-frequency EMFs with the plasminogen activator system was examined in BC cells. MCF-7 BC cells from 2 different sources were exposed to highly homogeneous 50-Hz EMFs. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction. In MCF-7 cells exposed to 1.2 mu T ENT expression of the urokinase plasminogen activator gene and of plasminogen-activator inhibitor-1 was markedly increased. The expression of the receptor for urokinase plasminogen activator was only marginally increased in I of the 2 tested cell lines and expression of the tissue plasminogen activator was at least slightly down-regulated in BC cells exposed to EMFs. EMFs may be able to increase the metastatic potential of breast tumors. The use of our newly established exposure system for EMFs may allow us to study the signaling processes involved in the induction of a metastatic phenotype of breast cancer cells."],["dc.identifier.doi","10.1111/IGC.0b013e31819f53ec"],["dc.identifier.isi","000266976600006"],["dc.identifier.pmid","19407555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17055"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1048-891X"],["dc.title","Exposure of MCF-7 Breast Cancer Cells to Electromagnetic Fields Up-Regulates the Plasminogen Activator System"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Schimming, H."],["dc.contributor.author","Kreienberg, Rolf"],["dc.contributor.author","Girgert, Rainer"],["dc.date.accessioned","2018-11-07T10:50:33Z"],["dc.date.available","2018-11-07T10:50:33Z"],["dc.date.issued","2004"],["dc.format.extent","109"],["dc.identifier.doi","10.1016/S1359-6349(04)90796-3"],["dc.identifier.isi","000202990100211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48684"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","1359-6349"],["dc.title","Antiproliferative activity of tamoxifen on MCF-7 breast cancer cells is modulated by weak electromagnetic field exposure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","169"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T11:16:21Z"],["dc.date.available","2018-11-07T11:16:21Z"],["dc.date.issued","2008"],["dc.description.abstract","Breast cancer is the most common malignancy of women in Western societies. The increasing exposure to electromagnetic fields has been suspected to contribute to the rising incidence of breast cancer in industrialized Countries. The majority of breast tumors is treated with the partial antiestrogen tamoxifen. Most tumors become resistant to tamoxifen in the course of treatment resulting in treatment failure. Electromagnetic fields reduce the efficacy of tamoxifen similar to tamoxifen resistance. In this study we investigated the mechanism by which electromagnetic fields influence the sensitivity to tamoxifen. In cells exposed to 1.2 mu T of a 50 Hz electromagnetic field gene expression of cofactors of the estrogen receptors was compared to sham exposed cells. Using a gene array technology several cofactors were found to be differentially expressed. The expression of the coactivators, SRC-I and AIB 1, and of two corepressors, N-Cor and SMRT, was quantified by RT-PCR. Both coactivators were expressed more strongly in the exposed cells while the expression of two corepressors decreased. The RNA analysis was confirmed by Western blots. The contradirectional changes in gene expression of coactivators and corepressors by electromagnetic fields results in a lower sensitivity to tamoxifen. Electromagnetic fields may contribute to the induction of tamoxifen resistance in vivo. Bioelectromagnetics 29:169-176, 2008. (C) 2007 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20387"],["dc.identifier.isi","000254479100002"],["dc.identifier.pmid","18027843"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54564"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Electromagnetic fields alter the expression of estrogen receptor cofactors in breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","237"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Bioelectromagnetics"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:44:20Z"],["dc.date.available","2018-11-07T08:44:20Z"],["dc.date.issued","2010"],["dc.description.abstract","The growth of estrogen-receptor positive breast cancer cells is inhibited by the pineal gland hormone, melatonin. Concern has been raised that power-line frequency and microwave electromagnetic fields (EMEs) could reduce the efficiency of melatonin on breast cancer cells. In this study we investigated the impact of EMIT's on the signal transduction of the high-affinity receptor MT1 M parental MCF-7 cells and MCF-7 cells transfected with the MT1 gene. The binding of the cAMP-responsive element binding (CREB) protein to a promoter sequence of BRCA-1 after stimulation with melatonin was analyzed by a gel-shift assay and the expression of four estrogen-responsive genes was measured in sham-exposed breast cancer cells and cells exposed to a sinusoidal 50Hz EMF of 1.2 mu T for 48 h. In sham-exposed cells, binding of CREB to the promoter of BRCA-1 was increased by estradiol and subsequently diminished by treatment with melatonin. In cells exposed to 1.2 mu T, 50Hz. EMF. binding of CREB was almost completely omitted. Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level. In contrast, in breast cancer cells transfected with MT1 exposed to 1.2 mu T of the 50Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment but for p21(WAF). the increase was not significant. These results convincingly prove the negative effect of EMF on the antiestrogenic effect of melatonin in breast cancer cells. Bioelectromagnetics 31:237-245, 2010. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/bem.20554"],["dc.identifier.isi","000276052600008"],["dc.identifier.pmid","19882681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20177"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0197-8462"],["dc.title","Signal Transduction of the Melatonin Receptor MT1 Is Disrupted in Breast Cancer Cells by Electromagnetic Fields"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1144"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","1149"],["dc.bibliographiccitation.volume","336"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Schimming, H."],["dc.contributor.author","Korner, W."],["dc.contributor.author","Grundker, A."],["dc.contributor.author","Hanf, Volker"],["dc.date.accessioned","2018-11-07T10:54:24Z"],["dc.date.available","2018-11-07T10:54:24Z"],["dc.date.issued","2005"],["dc.description.abstract","The incidence of breast cancer in western societies has been rising ever since the Second World War. Besides the exposure to a multitude of new chemical compounds, electromagnetic field exposure has been linked to breast cancer through a radiation-mediated anti-melatonin pathway. We investigated, whether low-frequency electromagnetic field exposure interferes with the anti-estrogenic activity of tamoxifen. Two different clones of the breast cancer cell line MCF-7 were exposed to highly homogeneous 50 Hz electromagnetic fields and IC50 values were calculated from dose-response curves of tamoxifen at various field intensities. An intensity-dependent shift of tamoxifen dose-response curves to higher concentrations with a maximal response at 1.2 mu T was observed. Hypothetically, electromagnetic field exposure could contribute to tamoxifen resistance observed in breast cancer after long-term treatment. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbrc.2005.08.243"],["dc.identifier.isi","000232515800022"],["dc.identifier.pmid","16168388"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49552"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0006-291X"],["dc.title","Induction of tamoxifen resistance in breast cancer cells by ELF electromagnetic fields"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S74"],["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.lastpage","S75"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T11:05:16Z"],["dc.date.available","2018-11-07T11:05:16Z"],["dc.date.issued","2007"],["dc.identifier.isi","000244865600280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52028"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Johann Ambrosius Barth Verlag Medizinverlage Heidelberg Gmbh"],["dc.publisher.place","Stuttgart"],["dc.relation.issn","0947-7349"],["dc.title","GnRH agonist Triptorelin reverts increased expression of the cofactors A1B1 and SRC-1 in breast cancer cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","23"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","31"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T08:27:21Z"],["dc.date.available","2018-11-07T08:27:21Z"],["dc.date.issued","2009"],["dc.description.abstract","Melatonin possesses anti-estrogenic effects on estrogen receptor expressing (ER+) breast cancer cells in culture by reducing cell cycle progression and cell proliferation. There is increasing agreement that on a cellular level the effects of melatonin are primarily induced by the membrane-bound receptor MT1. The participation of a second, nuclear receptor of the group of ligand-dependent transcription factors, called RZR alpha, is under debate. In this study we used a number of breast cancer cell lines differing in their expression of the estrogen receptor and the two known melatonin receptors. In MCF-7 breast cancer cells transfected with a vector carrying the MT1 gene (MCF-7Mel1a) binding of CREB-protein to the cAMP-responsive element of the breast cancer suppressing gene BRCA-1 was more strongly reduced by treatment with melatonin than in the parental cells. Expression of estrogen responsive genes was determined in serum-starved cells, cells stimulated for 16 hr with estradiol and cells subsequently treated with melatonin. Expression of BRCA-1, p53, p21(WAF) and c-myc were up-regulated by estradiol. Treatment of the stimulated cells with melatonin counteracted the increase induced by estradiol almost completely. The more MT1 a cell line expressed, the stronger was the reduction of the expression of the estradiol-induced genes. There was no correlation between the expression of the nuclear receptor RZR alpha and the effects of melatonin on these genes."],["dc.identifier.doi","10.1111/j.1600-079X.2009.00684.x"],["dc.identifier.isi","000267706300004"],["dc.identifier.pmid","19522736"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16188"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0742-3098"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Membrane-bound melatonin receptor MT1 down-regulates estrogen responsive genes in breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]