Kaulfuß, Silke

[["dc.bibliographiccitation.firstpage","2626"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","2633"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Stettner, Mark"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T10:58:18Z"],["dc.date.available","2018-11-07T10:58:18Z"],["dc.date.issued","2007"],["dc.description.abstract","In the prostate, estrogen receptor beta (ER beta), the preferred receptor for phytoestrogens, has features of a tumor suppressor. To investigate the mechanisms underlying the beneficial effects on prostate cancer of histone deacetylase inhibitor valproic acid (VPA) and phytoestrogen tectorigenin, we analyzed the expression of ER after tectorigenin or VPA treatment. For further functional analysis, we knocked down ER beta expression by RNA interference. LNCaP prostate cancer cells were treated with 5 mmol/L VPA or 100 mu mol/L tectorigenin and transfected with small interfering RNA (siRNA) against ER beta. Control transfections were done with luciferase (LUC) siRNA. Expression of ER beta was assessed by Western blot. mRNA expression was quantitated by real-time reverse transcription-PCR. Expression of ER beta mRNA and protein markedly increased after VPA or tectorigenin treatment. When ER beta was knocked down by siRNA, the expression of prostate-derived Ets factor, prostate-specific antigen, prostate cancer-specific indicator gene DD3(PCA3), insulin-like growth factor-1 receptor, the catalytic subunit of the telomerase, and ER beta was up-regulated and the tectorigenin effects were abrogated. ER beta levels were diminished in prostate cancer and loss of ER beta was associated with proliferation. Here, we show that siRNA-mediated knockdown of ER beta increases the expression of genes highly relevant to tumor cell proliferation. In addition, we show that one prominent result of treatment with VPA or tectorigenin is the up-regulation of ER beta resulting in antiproliferative effects. Thus, these drugs, by restoring the regulatory function of ER in tumor cells, could become useful in the intervention of prostate cancer."],["dc.identifier.doi","10.1158/1535-7163.MCT-07-0197"],["dc.identifier.isi","000250252100003"],["dc.identifier.pmid","17913855"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1535-7163"],["dc.title","The relevance of estrogen receptor-beta expression to the antiproliferative effects observed with histone deacetylase inhibitors and phytoestrogens in prostate cancer treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Oberthuer, R."],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T09:44:05Z"],["dc.date.available","2018-11-07T09:44:05Z"],["dc.date.issued","2014"],["dc.format.extent","44"],["dc.identifier.isi","000332306700145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34320"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Molecular mechanisms of receptor tyrosine kinase inhibition in colorectal cancer cells and indications for therapeutical options"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34971"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","34979"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gehrig, Julia"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Stettner, Mark"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T10:23:41Z"],["dc.date.available","2018-11-07T10:23:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Advanced prostate cancer can develop into castration-resistant prostate cancer (CRPC). This process is mediated either by intratumoral ligand synthesis or by mutations or aberrations of the androgen receptor (AR) or its cofactors. To date, no curative therapy for CRPC is available, as AR-targeted therapies eventually result in the development of resistance. The human prostate cancer cell line VCaP (vertebral cancer of the prostate) overexpresses AR and its splice variants (ARVs) as a mechanism of resistance to androgen-deprivation therapy (ADT) of external and intratumoral origin. In the present study, we demonstrate that stimulating estrogen receptor beta activity with the specific agonist 8 beta-VE2 in VCaP cells in successive stages of ADT induced a time-and dose-dependent decrease in cell survival and an increase in apoptosis. Furthermore, 8 beta-VE2 treatment reduced the overexpression of the AR as well as ARVs in VCaP cells under maximum ADT. Our results indicate that decreased survival of the androgen-dependent CRPC cells employing apoptosis together with the regulative effect on AR expression could have beneficial effects over current AR-targeting therapies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.18632/oncotarget.16496"],["dc.identifier.isi","000402051700085"],["dc.identifier.pmid","28380417"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14426"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42509"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Prospects of estrogen receptor beta activation in the treatment of castration-resistant prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","93"],["dc.bibliographiccitation.journal","Cancer Letters"],["dc.bibliographiccitation.lastpage","105"],["dc.bibliographiccitation.volume","407"],["dc.contributor.author","Oberthür, Rabea"],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Gehrig, Julia"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Halpape, Rovena"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Kaulfuß, Silke"],["dc.date.accessioned","2020-12-10T14:22:49Z"],["dc.date.available","2020-12-10T14:22:49Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.canlet.2017.08.009"],["dc.identifier.issn","0304-3835"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71746"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Simultaneous inhibition of IGF1R and EGFR enhances the efficacy of standard treatment for colorectal cancer by the impairment of DNA repair and the induction of cell death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Medical Genetics"],["dc.bibliographiccitation.lastpage","553"],["dc.bibliographiccitation.volume","59"],["dc.contributor.affiliation","Yigit, Gökhan; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Sheffer, Ruth; \r\n2\r\nDepartment of Human Genetics, Hadassah University Hospital, Jerusalem, Israel"],["dc.contributor.affiliation","Daana, Muhannad; \r\n3\r\nChild Development Institute, Clalit Health Services, Tel Aviv, Israel"],["dc.contributor.affiliation","Li, Yun; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Kaygusuz, Emrah; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Mor-Shakad, Hagar; \r\n2\r\nDepartment of Human Genetics, Hadassah University Hospital, Jerusalem, Israel"],["dc.contributor.affiliation","Altmüller, Janine; \r\n5\r\nCologne Center for Genomics (CCG), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany"],["dc.contributor.affiliation","Nürnberg, Peter; \r\n5\r\nCologne Center for Genomics (CCG), University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany"],["dc.contributor.affiliation","Douiev, Liza; \r\n2\r\nDepartment of Human Genetics, Hadassah University Hospital, Jerusalem, Israel"],["dc.contributor.affiliation","Kaulfuss, Silke; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Burfeind, Peter; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Wollnik, Bernd; \r\n1\r\nInstitute of Human Genetics, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Brockmann, Knut; \r\n7\r\nInterdisciplinary Pediatric Center for Children with Developmental Disabilities and Severe Chronic Disorders, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.author","Yigit, Gökhan"],["dc.contributor.author","Sheffer, Ruth"],["dc.contributor.author","Daana, Muhannad"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Kaygusuz, Emrah"],["dc.contributor.author","Mor-Shakad, Hagar"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Douiev, Liza"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Wollnik, Bernd"],["dc.date.accessioned","2021-07-05T14:57:45Z"],["dc.date.available","2021-07-05T14:57:45Z"],["dc.date.issued","2021"],["dc.date.updated","2022-05-21T14:18:33Z"],["dc.description.abstract","Background Developmental and epileptic encephalopathies (DEEs) represent a group of severe neurological disorders characterised by an onset of refractory seizures during infancy or early childhood accompanied by psychomotor developmental delay or regression. DEEs are genetically heterogeneous with, to date, more than 80 different genetic subtypes including DEE31 caused by heterozygous missense variants in DNM1 . Methods We performed a detailed clinical characterisation of two unrelated patients with DEE and used whole-exome sequencing to identify causative variants in these individuals. The identified variants were tested for cosegregation in the respective families. Results We excluded pathogenic variants in known, DEE-associated genes. We identified homozygous nonsense variants, c.97C>T; p.(Gln33 ) in family 1 and c.850C>T; p.(Gln284 ) in family 2, in the DNM1 gene, indicating that biallelic, loss-of-function pathogenic variants in DNM1 cause DEE. Conclusion Our finding that homozygous, loss-of-function variants in DNM1 cause DEE expands the spectrum of pathogenic variants in DNM1 . All parents who were heterozygous carriers of the identified loss-of-function variants were healthy and did not show any clinical symptoms, indicating that the type of mutation in DNM1 determines the pattern of inheritance."],["dc.description.abstract","Background Developmental and epileptic encephalopathies (DEEs) represent a group of severe neurological disorders characterised by an onset of refractory seizures during infancy or early childhood accompanied by psychomotor developmental delay or regression. DEEs are genetically heterogeneous with, to date, more than 80 different genetic subtypes including DEE31 caused by heterozygous missense variants in DNM1 . Methods We performed a detailed clinical characterisation of two unrelated patients with DEE and used whole-exome sequencing to identify causative variants in these individuals. The identified variants were tested for cosegregation in the respective families. Results We excluded pathogenic variants in known, DEE-associated genes. We identified homozygous nonsense variants, c.97C>T; p.(Gln33 ) in family 1 and c.850C>T; p.(Gln284 ) in family 2, in the DNM1 gene, indicating that biallelic, loss-of-function pathogenic variants in DNM1 cause DEE. Conclusion Our finding that homozygous, loss-of-function variants in DNM1 cause DEE expands the spectrum of pathogenic variants in DNM1 . All parents who were heterozygous carriers of the identified loss-of-function variants were healthy and did not show any clinical symptoms, indicating that the type of mutation in DNM1 determines the pattern of inheritance."],["dc.identifier","34172529"],["dc.identifier.doi","10.1136/jmedgenet-2021-107769"],["dc.identifier.pmid","34172529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87729"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/396"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/311"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | D02: Neue Mechanismen der genomischen Instabilität bei Herzinsuffizienz"],["dc.relation.eissn","1468-6244"],["dc.relation.issn","0022-2593"],["dc.relation.workinggroup","RG Wollnik"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","Loss-of-function variants in DNM1 cause a specific form of developmental and epileptic encephalopathy only in biallelic state"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1037"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","1049"],["dc.bibliographiccitation.volume","4"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Kampe, Rovena"],["dc.contributor.author","Meyer, Julia"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","König, Britta"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2019-07-09T11:54:26Z"],["dc.date.available","2019-07-09T11:54:26Z"],["dc.date.issued","2013"],["dc.description.abstract","Among the family of receptor tyrosine kinases (RTKs), platelet-derived growth factor receptor (PDGFR) has attracted increasing attention as a potential target of anti-tumor therapy in colorectal cancer (CRC). To study the function of PDGFRβ in CRC cell lines, SW480, DLD-1 and Caco-2 cells showing high PDGFRβ expression were used for receptor down-regulation by small interfering RNA (siRNA) and using the pharmacological inhibitor of PDGFRβ Ki11502. Blockade of PDGFRβ using both approaches led to moderate inhibition of proliferation and diminished activation of the downstream PI3K-signaling pathway in all three cell lines. Surprisingly, incubation with Ki11502 resulted in an arrest of SW480 cells in the G2 phase of the cell cycle, whereas the siRNA approach did not result in this effect. To address this difference, we analyzed the involvement of the PDGFRβ family member c-KIT in Ki11502 effectiveness, but siRNA and proliferation studies in SW480 and DLD-1 cells could not prove the involvement of c-KIT inactivation during Ki11502 treatment. Hence, an RTK activation antibody array on SW480 cells led us to the identification of the non-receptor tyrosine kinase SRC, which is inactivated after Ki11502 treatment but not after the siRNA approach. Further studies using the SRC-specific inhibitor PP2 showed that SRC inhibition upon treatment with the inhibitor Ki11502 is responsible for the observed effects of Ki11502 in SW480 and DLD-1 CRC cells. In summary, our results demonstrate that the inhibition of PDGFRβ alone using siRNA has only moderate cellular effects in CRC cell lines; however, the multi-target inhibition of PDGFRβ, c-KIT and SRC, e.g., using Ki11502, represents a promising therapeutic intervention for the treatment of CRC."],["dc.identifier.doi","10.18632/oncotarget.1085"],["dc.identifier.fs","598153"],["dc.identifier.pmid","23900414"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9173"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60657"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Blockade of the PDGFR family together with SRC leads to diminished proliferation of colorectal cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1115"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","1124"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Witt, Daria"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Neesen, Juergen"],["dc.contributor.author","Kaulfuss, Silke"],["dc.date.accessioned","2018-11-07T09:25:10Z"],["dc.date.available","2018-11-07T09:25:10Z"],["dc.date.issued","2013"],["dc.description.abstract","In this study, primary murine prostate cancer (PCa) cells were derived using the well-established TRAMP model. These PCa cells were treated with the histone deacetylase inhibitor, valproic acid (VPA), and we demonstrated that VPA treatment has an antimigrative, antiinvasive and antiproliferative effect on PCa cells. Using microarray analyses, we discovered several candidate genes that could contribute to the cellular effects we observed. In this study, we could demonstrate that VPA treatment of PCa cells causes the re-expression of cyclin D2, a known regulator that is frequently lost in PCa as we could show using immunohistochemical analyses on PCa specimens. We demonstrate that VPA specifically induces the re-expression of cyclin D2, one of the highly conserved D-type cyclin family members, in several cancer cell lines with weak or no cyclin D2 expression. Interestingly, VPA treatment had no effect in fibroblasts, which typically have high basal levels of cyclin D2 expression. The re-expression of cyclin D2 observed in PCa cells is activated by increased histone acetylation in the promoter region of the Ccnd2 gene and represents one underlying molecular mechanism of VPA treatment that inhibits the proliferation of cancer cells. Altogether, our results confirm that VPA is an anticancer therapeutic drug for the treatment of tumors with epigenetically repressed cyclin D2 expression."],["dc.identifier.doi","10.1093/carcin/bgt019"],["dc.identifier.isi","000318646000021"],["dc.identifier.pmid","23349020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","Valproic acid inhibits the proliferation of cancer cells by re-expressing cyclin D2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13591"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","13606"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dierks, Sascha"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Schmidt, Thomas"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Kaulfuß, Silke"],["dc.date.accessioned","2021-11-22T14:31:34Z"],["dc.date.available","2021-11-22T14:31:34Z"],["dc.date.issued","2015-05-30"],["dc.description.abstract","The focal adhesion protein leupaxin (LPXN) is overexpressed in a subset of prostate cancers (PCa) and is involved in the progression of PCa. In the present study, we analyzed the LPXN-mediated adhesive and cytoskeletal changes during PCa progression. We identified an interaction between the actin-binding protein caldesmon (CaD) and LPXN and this interaction is increased during PCa cell migration. Furthermore, knockdown of LPXN did not affect CaD expression but reduced CaD phosphorylation. This is known to destabilize the affinity of CaD to F-actin, leading to dynamic cell structures that enable cell motility. Thus, downregulation of CaD increased migration and invasion of PCa cells. To identify the kinase responsible for the LPXN-mediated phosphorylation of CaD, we used data from an antibody array, which showed decreased expression of TGF-beta-activated kinase 1 (TAK1) after LPXN knockdown in PC-3 PCa cells. Subsequent analyses of the downstream kinases revealed the extracellular signal-regulated kinase (ERK) as an interaction partner of LPXN that facilitates CaD phosphorylation during LPXN-mediated PCa cell migration. In conclusion, we demonstrate that LPXN directly influences cytoskeletal dynamics via interaction with the actin-binding protein CaD and regulates CaD phosphorylation by recruiting ERK to highly dynamic structures within PCa cells."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KA2946/1-1, KA2946/1-2]"],["dc.identifier.doi","10.18632/oncotarget.3792"],["dc.identifier.fs","613073"],["dc.identifier.isi","000359009400054"],["dc.identifier.pmid","26079947"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93389"],["dc.language","eng"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.access","openAccess"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject","prostate cancer, leupaxin, caldesmon, migration"],["dc.subject.mesh","Actins"],["dc.subject.mesh","Calmodulin-Binding Proteins"],["dc.subject.mesh","Cell Adhesion"],["dc.subject.mesh","Cell Adhesion Molecules"],["dc.subject.mesh","Cell Line, Tumor"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Disease Progression"],["dc.subject.mesh","Gene Knockdown Techniques"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Mitogen-Activated Protein Kinase 1"],["dc.subject.mesh","Mitogen-Activated Protein Kinase 3"],["dc.subject.mesh","Phosphoproteins"],["dc.subject.mesh","Phosphorylation"],["dc.subject.mesh","Prostatic Neoplasms"],["dc.subject.mesh","Signal Transduction"],["dc.subject.mesh","Transfection"],["dc.title","Leupaxin stimulates adhesion and migration of prostate cancer cells through modulation of the phosphorylation status of the actin-binding protein caldesmon."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","16951"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","16961"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Unterkircher, Valerie"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2019-07-09T11:45:18Z"],["dc.date.available","2019-07-09T11:45:18Z"],["dc.date.issued","2018"],["dc.description.abstract","Novel treatments for castration-resistant prostate cancer (CRPC) such as abiraterone acetate (AA) or enzalutamide effectively target the androgen pathway to arrest aberrant signalling and cell proliferation. Testosterone is able to inhibit tumour cell growth in CRPC. Estrogen receptor-beta (ERβ) binds the testosteronemetabolites 3β-androstanediol and 3α-androstanediol in parallel to the canonical estradiol. In the prostate it is widely accepted that ERβ regulates estrogen signalling, mediating anti-proliferative effects. We used the prostate cancer cell lines LNCaP, PC-3, VCaP, and the non-neoplastic BPH-1. VCaP cells were treated with 1 nmol/L testosterone over 20 passages, yielding the cell line VCaPrev, sensitive to hormone therapies. In contrast, LNCaP cells were grown for more than 100 passages yielding a high passage therapy resistant cell line (hiPLNCaP). VCaP and hiPLNCaP cell lines were treated with 5 μmol/L AA for more than 20 passages, respectively, generating the AAtolerant- subtypes VCaPAA and hiPLNCaPAA. Cell lines were treated with testosterone, dihydrotestosterone (DHT), R1881, and the androgen-metabolites 3β-androstanediol and 3α-androstanediol. 3β-androstanediol or 3α-androstanediol significantly reduced proliferation in all cell lines except the BPH-1 and androgen receptor-negative PC-3 and markedly downregulated AR and estrogen receptor alpha (ERα). Whereas ERβ expression was increased in all cell lines except BPH-1 or PC-3. In summary, 3β-adiol or 3α-adiol, as well as DHT and R1881, significantly reduced tumour cell growth in CRPC cells. Thus, these compounds represent novel potential therapeutic approaches to overcome drug-resistance in CRPC, especially with regard to AR-V7 function in therapy resistance. Furthermore, these data confirm the tumour suppressor properties of ERβ in CRPC."],["dc.identifier.doi","10.18632/oncotarget.24763"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59207"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","Testosterone metabolites inhibit proliferation of castration- and therapy-resistant prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","559"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","Clinical Genetics"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","101"],["dc.contributor.affiliation","Gönenc, Ipek Ilgin; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Elcioglu, Nursel H.; 2\r\nDepartment of Pediatric Genetics\r\nMarmara University Medical School\r\nIstanbul Turkey"],["dc.contributor.affiliation","Martinez Grijalva, Carolina; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Aras, Seda; 4\r\nDepartment of Pediatric Haematology and Oncology\r\nMarmara University Medical School\r\nIstanbul Turkey"],["dc.contributor.affiliation","Großmann, Nadine; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Praulich, Inka; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Altmüller, Janine; 5\r\nCologne Center for Genomics (CCG)\r\nUniversity of Cologne\r\nCologne Germany"],["dc.contributor.affiliation","Kaulfuß, Silke; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Li, Yun; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Nürnberg, Peter; 5\r\nCologne Center for Genomics (CCG)\r\nUniversity of Cologne\r\nCologne Germany"],["dc.contributor.affiliation","Burfeind, Peter; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Yigit, Gökhan; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.author","Gönenc, Ipek Ilgin"],["dc.contributor.author","Elcioglu, Nursel H."],["dc.contributor.author","Martinez Grijalva, Carolina"],["dc.contributor.author","Aras, Seda"],["dc.contributor.author","Großmann, Nadine"],["dc.contributor.author","Praulich, Inka"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Yigit, Gökhan"],["dc.date.accessioned","2022-04-01T10:00:24Z"],["dc.date.available","2022-04-01T10:00:24Z"],["dc.date.issued","2022"],["dc.date.updated","2022-06-14T22:49:33Z"],["dc.description.abstract","Abstract Bloom syndrome (BS) is an autosomal recessive disorder with characteristic clinical features of primary microcephaly, growth deficiency, cancer predisposition, and immunodeficiency. Here, we report the clinical and molecular findings of eight patients from six families diagnosed with BS. We identified causative pathogenic variants in all families including three different variants in BLM and one variant in RMI1. The homozygous c.581_582delTT;p.Phe194 and c.3164G>C;p.Cys1055Ser variants in BLM have already been reported in BS patients, while the c.572_573delGA;p.Arg191Lysfs 4 variant is novel. Additionally, we present the detailed clinical characteristics of two cases with BS in which we previously identified the biallelic loss‐of‐function variant c.1255_1259delAAGAA;p.Lys419Leufs 5 in RMI1. All BS patients had primary microcephaly, intrauterine growth delay, and short stature, presenting the phenotypic hallmarks of BS. However, skin lesions and upper airway infections were observed only in some of the patients. Overall, patients with pathogenic BLM variants had a more severe BS phenotype compared to patients carrying the pathogenic variants in RMI1, especially in terms of immunodeficiency, which should be considered as one of the most important phenotypic characteristics of BS."],["dc.description.abstract","Phenotypic features of Bloom syndrome differ in severity between patients carrying pathogenic variants in BLM and RMI1. image"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Research Group FOR 2800 “Chromosome Instability: Cross‐talk of DNA replication stress and mitotic dysfunction”, SP5 and SPZ"],["dc.description.sponsorship","German Center for Cardiovascular Research (DZHK, partner site Göttingen)"],["dc.description.sponsorship","Germany's Excellence Strategy, Cluster of Excellence \"Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells\" (MBExC; EXC 2067/1‐390729940)"],["dc.identifier.doi","10.1111/cge.14125"],["dc.identifier.pmid","35218564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105419"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/455"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1399-0004"],["dc.relation.issn","0009-9163"],["dc.relation.workinggroup","RG Wollnik"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Phenotypic spectrum of BLM‐ and RMI1‐related Bloom syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]