Burfeind, Peter

[["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","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","1606"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Molecular Endocrinology"],["dc.bibliographiccitation.lastpage","1621"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Grzmil, Michal"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Neesen, Juergen"],["dc.contributor.author","Bubendorf, Lukas"],["dc.contributor.author","Glass, Andrew G."],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:13:42Z"],["dc.date.available","2018-11-07T11:13:42Z"],["dc.date.issued","2008"],["dc.description.abstract","In the present study, we demonstrate that leupaxin mRNA is overexpressed in prostate cancer (PCa) as compared with normal prostate tissue by using cDNA arrays and quantitative RT-PCR analyses. Moderate to strong expression of leupaxin protein was detected in approximately 22% of the PCa tissue sections analyzed, and leupaxin expression intensities were found to be significantly correlated with Gleason patterns/scores. In addition, different leupaxin expression levels were observed in PCa cell lines, and at the subcellular level, leupaxin was usually localized in focal adhesion sites. Furthermore, mutational analysis and transfection experiments of LNCaP cells using different green fluorescent protein-leupaxin constructs demonstrated that leupaxin contains functional nuclear export signals in its LD3 and LD4 motifs, thus shuttling between the cytoplasm and the nucleus. We could also demonstrate for the first time that leupaxin interacts with the androgen receptor in a ligand-dependent manner and serves as a transcriptional activator of this hormone receptor in PCa cells. Down-regulation of leupaxin expression using RNA interference in LNCaP cells resulted in a high rate of morphological changes, detachment, spontaneous apoptosis, and a reduction of prostate-specific antigen secretion. In contrast, knockdown of leupaxin expression in androgen-independent PC-3 and DU 145 cells induced a significant decrease of both the invasive capacity and motility. Our results therefore indicate that leupaxin could serve as a potential progression marker for a subset of PCa and may represent a novel coactivator of the androgen receptor. Leupaxin could function as a putative target for therapeutic interventions of a subset of advanced PCa."],["dc.identifier.doi","10.1210/me.2006-0546"],["dc.identifier.isi","000257144500008"],["dc.identifier.pmid","18451096"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53958"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0888-8809"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Leupaxin, a novel coactivator of the androgen receptor, is expressed in prostate cancer and plays a role in adhesion and invasion of prostate carcinoma cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33426"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","33437"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schallenberg, Simon"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Honecker, Friedemann"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2018-11-07T09:50:04Z"],["dc.date.available","2018-11-07T09:50:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Germ cell tumors (GCTs) are the most common malignancies in young men. Most patients with GCT can be cured with cisplatin-based combination chemotherapy, even in metastatic disease. In case of therapy resistance, prognosis is usually poor. We investigated the potential of N-cadherin inhibition as a therapeutic strategy. We analyzed the GCT cell lines NCCIT, NTERA-2, TCam-2, and the cisplatin-resistant sublines NCCIT-R and NTERA-2R. Effects of a blocking antibody or siRNA against N-cadherin on proliferation, migration, and invasion were investigated. Mouse xenografts of GCT cell lines were analyzed by immunohistochemistry for N-cadherin expression. All investigated GCT cell lines were found to express N-cadherin protein in vitro and in vivo. Downregulation of N-cadherin in vitro leads to a significant inhibition of proliferation, migration, and invasion. N-cadherin-downregulation leads to a significantly higher level of pERK. N-cadherin-inhibition resulted in significantly higher rates of apoptotic cells in caspase-3 staining. Expression of N-cadherin is preserved in cisplatin-resistant GCT cells, pointing to an important physiological role in cell survival. N-cadherin-downregulation results in a significant decrease of proliferation, migration, and invasion and stimulates apoptosis in cisplatin-naive and resistant GCT cell lines. Therefore, targeting N-cadherin may be a promising therapeutic approach, particularly in cisplatin-resistant, therapy refractory and metastatic GCT."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.18632/oncotarget.5288"],["dc.identifier.isi","000363186600100"],["dc.identifier.pmid","26451610"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35638"],["dc.notes.intern","Merged 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.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Role of N-cadherin in proliferation, migration, and invasion of germ cell tumours"],["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"]]