Bauerschmitz, Gerd Johannes

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[["dc.bibliographiccitation.firstpage","914"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Der Gynäkologe"],["dc.bibliographiccitation.lastpage","919"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Bauerschmitz, G. J."],["dc.contributor.author","Hellriegel, M."],["dc.contributor.author","Emons, G."],["dc.date.accessioned","2020-12-10T14:08:43Z"],["dc.date.available","2020-12-10T14:08:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00129-017-4156-6"],["dc.identifier.eissn","1433-0393"],["dc.identifier.issn","0017-5994"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70534"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Palliative Konzepte beim Endometrium‑, Zervix- und Vulvakarzinom"],["dc.title.alternative","Palliative concepts for endometrial, cervical and vulvar cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2713"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","2721"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Schubert, Antje"],["dc.contributor.author","Emons, Guenter"],["dc.date.accessioned","2018-11-07T10:13:49Z"],["dc.date.available","2018-11-07T10:13:49Z"],["dc.date.issued","2016"],["dc.description.abstract","S100 calcium binding protein A4 (S100A4) and cysteine-rich angiogenic inducer 61 (CYR61) play important roles in epithelial-mesenchymal-transition (EMT), invasion and metastasis by promoting cancer cell motility. Recently we were able to show that invasion of GnRH receptor-positive breast cancer cells is time- and dose-dependently reduced by GnRH analogs. We have now analyzed whether GnRH treatment affects S100A4 and CYR61 in mesenchymal transformed breast cancer cells. S100A4 and CYR61 expression was analyzed using RT-PCR. Invasion was quantified by assessment of breast cancer cell migration rate through an artificial basement membrane. The role of S100A4 and CYR61 in invasion of breast cancer cells was analyzed by neutralizing their biological activity. Expression of S100A4, CYR61 and GnRH receptor in human breast cancers, normal and other non-malignant breast tissues was analyzed by immunohistochemistry. Invasion and expression of S100A4 and CYR61 in MDA-MB-231 breast cancer cells were significant higher as compared with MCF-7 breast cancer cells. Invasion and expression of S100A4 and CYR61 were significantly increased in mesenchymal transformed MCF-7 cells (MCF-7-EMT). The increased invasion of MCF-7-EMT cells could be reduced by anti-S100A4 and anti-CYR61 antibodies. In addition, invasion of MDA-MB-231 cells was decreased by anti-S100A4 and anti-CYR61 antibodies. Treatment of MCF-7-EMT and MDA-MB-231 cells with GnRH agonist Triptorelin resulted in a significant decrease of invasion and expression of S100A4 and CYR61. Both, S100A4 and CYR61 were found highly expressed in biopsy specimens of breast hyperplasia and malignant breast cancers. GnRH receptor expression was detectable in approximately 71% of malignant breast cancers. Our findings suggest that S100A4 and CYR61 play major roles in breast cancer invasion. Both, invasion and expression of S100A4 and CYR61 can be inhibited by GnRH treatment."],["dc.identifier.doi","10.3892/ijo.2016.3491"],["dc.identifier.isi","000375807900049"],["dc.identifier.pmid","27098123"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40506"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1791-2423"],["dc.relation.issn","1019-6439"],["dc.title","Invasion and increased expression of S100A4 and CYR61 in mesenchymal transformed breast cancer cells is downregulated by GnRH"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","41"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Breast Cancer Research and Treatment"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","152"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Knapp, Juliane"],["dc.contributor.author","Schmidt, Elena"],["dc.contributor.author","Olbrich, Theresa"],["dc.contributor.author","Emons, Gunter"],["dc.date.accessioned","2018-11-07T09:55:28Z"],["dc.date.available","2018-11-07T09:55:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Recently we have shown that breast cancer cell invasion was dramatically increased when co-cultured with MG63 cells. In addition we have generated mesenchymal transformed MCF-7 breast cancer cells (MCF-7-EMT), showing significantly increased invasion in contrast to wild type MCF-7 cells (MCF-7 WT). In this study we have analyzed whether stromal derived factor-1 (SDF-1) is responsible for MCF-7 and T-47-D breast cancer cell invasion and epithelial-mesenchymal-transition (EMT). In addition we have analyzed whether kisspeptin-10 (KP-10) treatment affects SDF-1-induced invasion and EMT. Invasion was quantified by assessment of MCF-7 and T-47-D breast cancer cell migration rate through an artificial basement membrane in a modified Boyden chamber during co-culture with MG63 cells or after treatment with SDF-1 alpha, SDF-1 beta or the combination of both isoforms. Induction of EMT was verified by analysis of protein expression of epithelial marker E-cadherin (CDH1) and mesenchymal markers N-cadherin (CDH2) and Vimentin (VIM). The role of SDF-1 for invasion and induction of EMT in breast cancer cells was analyzed by blocking SDF-1 secretion during co-culture with MG63 cells. In addition effects of KP-10 treatment on SDF-1-induced invasion and EMT were analyzed. Breast cancer cell invasion was significantly increased when co-cultured with MG63 cells. During co-culture SDF-1 protein expression of MG63 cells was significantly induced. The increased breast cancer cell invasion could be blocked by anti-SDF-1 antibodies. Treatment of breast cancer cells in monoculture (without MG63) with SDF-1 alpha, SDF-1 beta or the combination of both isoforms resulted in a significant escalation of breast cancer cell invasion and induction of EMT. Protein expression of mesenchymal markers CDH2 and VIM was clearly elevated, whereas protein expression of epithelial marker CDH1 was clearly decreased. The SDF-1-induced increase of cell invasion was significantly reduced after treatment with KP-10. In addition, induction of EMT was inhibited. Furthermore, protein expression of the binding site of SDF-1, CXC-motive-chemokine receptor 4 (CXCR-4), was reduced by KP-10. Treatment of MCF-7-EMT cells with KP-10 resulted in a significant drop of cell invasion and CXCR-4 protein expression. Our findings suggest that SDF-1 plays a major role in breast cancer invasion and EMT. SDF-1-induced invasion and EMT can be inhibited by KP-10 treatment by down-regulating CXCR-4 expression."],["dc.description.sponsorship","Deutsche Krebshilfe-Dr. Mildred Scheel Stiftung"],["dc.identifier.doi","10.1007/s10549-015-3463-7"],["dc.identifier.isi","000356248900005"],["dc.identifier.pmid","26062751"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36743"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1573-7217"],["dc.relation.issn","0167-6806"],["dc.title","Inhibition of SDF-1/CXCR4-induced epithelial-mesenchymal transition by kisspeptin-10"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

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