Emons, Günter

[["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Peick, D."],["dc.contributor.author","Fister, Stefanie"],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T08:46:28Z"],["dc.date.available","2018-11-07T08:46:28Z"],["dc.date.issued","2010"],["dc.format.extent","36"],["dc.identifier.isi","000274745200095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20699"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","Strengthening of GnRH-II antagonist-induced apoptosis via combined treatment of 40H-Tamoxifen in a case estrogen-receptor-positive breast cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1223"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1229"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Eicke, Nicola"],["dc.contributor.author","Guenthert, Andreas R."],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T09:01:26Z"],["dc.date.available","2018-11-07T09:01:26Z"],["dc.date.issued","2006"],["dc.description.abstract","The majority of human endometrial and ovarian cancers express receptors for GnRH type I (GnRH-I). Their proliferation is time- and dose-dependently reduced by GnRH-I and its analogs. GnRH-I analogs activate a phosphotyrosine-phosphatase (PTP) and inhibit EGF-induced mitogenic signal transduction. Recently we found that GnRH type II (GnRH-II) and its agonist [D-Lys(6)]GnRH-II also have antiproliferative effects on these tumor cells which are significantly greater than those of GnRH-I agonists. In a more recent study, we showed that the antiproliferative activity of GnRH-II on human endometrial and ovarian cancer cell lines is not mediated through the GnRH-I receptor. The underlying signal transduction mechanisms of GnRH-III are still unknown. In this study we showed that the mitogenic effects of growth factors in endometrial and ovarian cancer cell lines were counteracted by GnRH-II agonist [D-LyS(6)]GnRH-II, indicating an interaction with the mitogenic signal transduction. We showed that [D-LyS6]GnRH-III reduces EGF-induced auto-tyrosine-phosphorylation of EGF-receptors via activation of a PTP and that EGF-induced activation of mitogen-activated protein kinase was blocked in cells treated with [D-Lys(6)]GnRH-H. Furthermore, EGF-induced expression of the immediate early gene c-fos was inhibited by treatment with [D-Lys(6)]GnRH-II. After knock-out of GnRH-I receptor expression, GnRH-H agonist [D-LyS(6)]GnRH-II still activated PTP and inhibited the EGF-induced mitogenic signal transduction. These data indicate, that the effects of GnRH-H are not due to a cross-reaction with the GnRH-I receptor. In conclusion these data suggest that the si naling of GnRH-II agonist [D-LyS(6)]GnRH-H is comparable to that of GnRH-I analogs."],["dc.identifier.isi","000241476100022"],["dc.identifier.pmid","17016655"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24424"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Professor D A Spandidos"],["dc.relation.issn","1019-6439"],["dc.title","GnRH-II agonist [D-Lys(6)]GnRH-II inhibits the EGF-induced mitogenic signal transduction in human endometrial and ovarian 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","1334"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Journal of Obstetrics and Gynaecology Research"],["dc.bibliographiccitation.lastpage","1342"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Wokoun, Ulrike"],["dc.contributor.author","Hellriegel, Martin"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2020-12-10T18:29:03Z"],["dc.date.available","2020-12-10T18:29:03Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1111/jog.13980"],["dc.identifier.eissn","1447-0756"],["dc.identifier.issn","1341-8076"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76505"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Inhibition of aerobic glycolysis enhances the anti‐tumor efficacy of Zoptarelin Doxorubicin in triple‐negative breast cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hellinger, Johanna W."],["dc.contributor.author","Schömel, Franziska"],["dc.contributor.author","Buse, Judith V."],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-04-14T08:31:47Z"],["dc.date.available","2021-04-14T08:31:47Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41598-020-74838-8"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17824"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83712"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","65"],["dc.bibliographiccitation.journal","Reproductive biology and endocrinology"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2019-07-09T11:41:55Z"],["dc.date.available","2019-07-09T11:41:55Z"],["dc.date.issued","2003"],["dc.description.abstract","The expression of GnRH (GnRH-I, LHRH) and its receptor as a part of an autocrine regulatory system of cell proliferation has been demonstrated in a number of human malignant tumors, including cancers of the ovary. The proliferation of human ovarian cancer cell lines is time- and dose-dependently reduced by GnRH and its superagonistic analogs. The classical GnRH receptor signal-transduction mechanisms, known to operate in the pituitary, are not involved in the mediation of antiproliferative effects of GnRH analogs in these cancer cells. The GnRH receptor rather interacts with the mitogenic signal transduction of growth-factor receptors and related oncogene products associated with tyrosine kinase activity via activation of a phosphotyrosine phosphatase resulting in downregulation of cancer cell proliferation. In addition GnRH activates nucleus factor ?B (NF?B) and protects the cancer cells from apoptosis. Furthermore GnRH induces activation of the c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) pathway independent of the known AP-1 activators, protein kinase (PKC) or mitogen activated protein kinase (MAPK/ERK). Recently it was shown that human ovarian cancer cells express a putative second GnRH receptor specific for GnRH type II (GnRH-II). The proliferation of these cells is dose- and time-dependently reduced by GnRH-II in a greater extent than by GnRH-I (GnRH, LHRH) superagonists..."],["dc.identifier.doi","10.1186/1477-7827-1-65"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58547"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616.99"],["dc.subject.ddc","618.1"],["dc.title","Role of gonadotropin-releasing hormone (GnRH) in ovarian cancer ; Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncology Reports"],["dc.bibliographiccitation.lastpage","554"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Ziegler, Elke"],["dc.contributor.author","Olbrich, Teresa"],["dc.contributor.author","Emons, Guenter"],["dc.contributor.author","Gruendker, Carsten"],["dc.date.accessioned","2018-11-07T09:28:41Z"],["dc.date.available","2018-11-07T09:28:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Kisspeptins are peptides derived from the metastasis suppressor gene KISS1 interacting with GPR54 as their corresponding receptor. The KISS1/GPR54 system is one regulator of cellular motility mechanisms leading to decreased migration and invasion. Its role in cell proliferation processes is not clearly understood. In this study, breast cancer cell lines, T47D, ZR75-1, MDA-MB-231, MDA-MB-435s, MDA-MB-453, HCC 70, HCC 1806, HCC 1937 and MCF-7, were investigated for their endogenous GPR54 expression by immunocytochemistry, RT-PCR and western blot analysis. The effect of kisspeptin-10 on proliferation was measured in MDA-MB-231, MDA-MB-435s, HCC 1806 and MCF-7 cells. Further experiments on proliferation were carried out with cells transfected with GPR54. All of the tested breast cancer cell lines expressed GPR54 in different amounts. No effects on proliferation were detected in the breast cancer cells expressing the receptor endogenously. In transfected neuronal cells overexpressing GPR54, proliferation was significantly inhibited by kisspeptin-10. The results indicate that the antiproliferative action of kisspeptin depends on the nature of GPR54 expression. The effect was detected in an artificial system of cells transfected with GPR54 and not in cells expressing the receptor endogenously. Thus, the antiproliferative action of kisspeptin seems not to be important for pathophysiological processes."],["dc.description.sponsorship","Deutsche Krebshilfe, Dr Mildred Scheel Stiftung"],["dc.identifier.doi","10.3892/or.2012.2135"],["dc.identifier.isi","000313605100021"],["dc.identifier.pmid","23152107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1021-335X"],["dc.title","Antiproliferative effects of kisspeptin-10 depend on artificial GPR54 (KISS1R) expression levels"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Experimental and Clinical Endocrinology & Diabetes"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Block, M."],["dc.contributor.author","Fister, Stefanie"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Guenthert, Andreas R."],["dc.date.accessioned","2018-11-07T11:05:14Z"],["dc.date.available","2018-11-07T11:05:14Z"],["dc.date.issued","2007"],["dc.format.extent","S74"],["dc.identifier.isi","000244865600278"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52022"],["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","Mechanisms of GnRH-induced resensitizing of breast cancer cells with secondary anti-estrogen resistance"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","187"],["dc.bibliographiccitation.journal","Frontiers in Endocrinology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gründker, Carsten"],["dc.contributor.author","Emons, Günter"],["dc.date.accessioned","2019-07-09T11:43:36Z"],["dc.date.available","2019-07-09T11:43:36Z"],["dc.date.issued","2017"],["dc.description.abstract","In several human malignant tumors of the urogenital tract, including cancers of the endometrium, ovary, urinary bladder, and prostate, it has been possible to identify expression of gonadotropin-releasing hormone (GnRH) and its receptor as part of an autocrine system, which regulates cell proliferation. The expression of GnRH receptor has also been identified in breast cancers and non-reproductive cancers such as pancreatic cancers and glioblastoma. Various investigators have observed dose- and timedependent growth inhibitory effects of GnRH agonists in cell lines derived from these cancers. GnRH antagonists have also shown marked growth inhibitory effects on most cancer cell lines. This indicates that in the GnRH system in cancer cells, there may not be a dichotomy between GnRH agonists and antagonists. The well-known signaling mechanisms of the GnRH receptor, which are present in pituitary gonadotrophs, are not involved in forwarding the antiproliferative effects of GnRH analogs in cancer cells. Instead, the GnRH receptor activates a phosphotyrosine phosphatase (PTP) and counteracts with the mitogenic signal transduction of growth factor receptors, which results in a reduction of cancer cell proliferation. The PTP activation, which is induced by GnRH, also inhibits G-protein-coupled estrogen receptor 1 (GPER), which is a membrane- bound receptor for estrogens. GPER plays an important role in breast cancers, which do not express the estrogen receptor α (ERα). In metastatic breast, ovarian, and endometrial cancer cells, GnRH reduces cell invasion in vitro, metastasis in vivo, and the increased expression of S100A4 and CYR61. All of these factors play important roles in epithelial–mesenchymal transition. This review will summarize the present state of knowledge about the GnRH receptor and its signaling in human cancers."],["dc.identifier.doi","10.3389/fendo.2017.00187"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58927"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-2392"],["dc.relation.issn","1664-2392"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The Role of Gonadotropin-Releasing Hormone in Cancer Cell Proliferation and Metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","725"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cellular Biochemistry"],["dc.bibliographiccitation.lastpage","735"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hofbauer, L. C."],["dc.date.accessioned","2018-11-07T10:33:20Z"],["dc.date.available","2018-11-07T10:33:20Z"],["dc.date.issued","2002"],["dc.description.abstract","The anti-resorptive effects of estrogen on bone metabolism are thought to be mediated through modulation of paracrine factors produced by osteoblastic lineage cells that act on osteoclastic lineage cells. Receptor activator of nuclear factor-kappaB ligand (RANKL) is the essential factor for osteoclast formation and activation and enhances bone resorption. By contrast, osteoprotegerin (OPG), which is produced by osteoblastic lineage cells acts as a decoy receptor that neutralizes RANKL and prevents bone loss. Recently, 17beta-estradiol was found to stimulate OPG mRNA levels and protein secretion in a human osteoblastic cell line through activation of the estrogen receptor (ER)-alpha. In this study, we assessed the effects of the phytoestrogen genistein on OPG mRNA steady state levels (by semiquantitative RT-PCIR and Northern analysis) and protein production (by ELISA) in primary human trabecular osteoblasts (hOB) obtained from healthy donors. Genistein increased OPG mRNA levels and protein secretion by hOB cells by up to two- to six-fold in a dose- (P< 0.0001) and time-dependent (P< 0.0001) fashion with a maximum effect at 10(-7) M. Co-treatment with the pure ER antagonist ICI 182,780 completely abrogated the stimulatory effects of genistein on OPG protein secretion, indicating that these effects were specific and directly mediated through the ER. Pre-treatment with genistein partially prevented the inhibitory effects of the glucocorticoid dexamethasone on OPG mRNA and protein production. The stimulation of OPG mRNA levels by genistein was not affected by the protein synthesis inhibitor, cycloheximide and was shown to be due to enhancement of OPG gene transcription. In conclusion, our data suggest that the phytoestrogen genistein is capable of upregulating the production of OPG by human osteoblasts. Thus, dietary sources of phytoestrogens may help to prevent bone resorption and bone loss by enhanced osteoblastic production of OPG. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jcb.10087"],["dc.identifier.isi","000173618800008"],["dc.identifier.pmid","11835398"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44583"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0730-2312"],["dc.title","Phytoestrogen genistein stimulates the production of osteoprotegerin by human trabecular osteoblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1427"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Journal of Clinical Endocrinology & Metabolism"],["dc.bibliographiccitation.lastpage","1430"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Gunthert, Andreas R."],["dc.contributor.author","Millar, R. P."],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2018-11-07T10:31:23Z"],["dc.date.available","2018-11-07T10:31:23Z"],["dc.date.issued","2002"],["dc.description.abstract","Recently it was shown that a second GnRH system exists in primates. This study was conducted to investigate whether or not the receptor specific for GnRH type II is expressed in human endometrial and ovarian cancer cells and whether or not GnRH-II has effects on tumor cell proliferation. Expression of GnRH-II receptor mRNA in endometrial and ovarian cancer cell lines was demonstrated using RT-PCR and Southern blot analysis. The proliferation of these cell lines was dose- and time-dependently reduced by native GnRH-II. These effects were significantly more potent than the antiproliferative effects of equimolar doses of GnRH-I agonist Triptorelin (p < 0.001). In the GnRH-II receptor positive but GnRH-I receptor negative ovarian cancer cell line SK-OV-3 native GnRH-II but not GnRH-I agonist Triptorelin had antiproliferative effects."],["dc.identifier.doi","10.1210/jc.87.3.1427"],["dc.identifier.isi","000174620600074"],["dc.identifier.pmid","11889221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44098"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0021-972X"],["dc.title","Expression of gonadotropin-releasing hormone II (GnRH-II) receptor in human endometrial and ovarian cancer cells and effects of GnRH-II on tumor cell proliferation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]