Kaulfuß, Silke

[["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","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","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","877"],["dc.bibliographiccitation.journal","INTERNATIONAL JOURNAL OF ONCOLOGY"],["dc.bibliographiccitation.lastpage","884"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Possner, Maria"],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Schulz, Wolfgang"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2019-07-10T08:13:32Z"],["dc.date.available","2019-07-10T08:13:32Z"],["dc.date.issued","2008"],["dc.description.abstract","The function of the androgen-regulated homeobox protein NKX3.1 in prostate cancer is controversial. NKX3.1 is necessary for correct prostate development and undergoes frequent allelic loss in prostate cancer. However, no mutations occur in the coding region and some particularly aggressive cancers over-express the protein. Nevertheless NKX3.1 is often referred to as candidate tumor suppressor gene. Recent findings suggest a function in protection against oxidative damage involved in prostate carcinogenesis. Thus NKX3.1 may act differently at various stages of prostate cancer. Unlike a classical tumor suppressor NKX3.1 is up-regulated by androgens and down-regulated by phytoestrogens. In this study we performed RNAi based functional analysis by knocking down NKX3.1 expression in LNCaP prostate cancer cells and analyzing the impact of NKX3.1 on gene expression and cell proliferation. Knockdown of NKX3.1 evoked a massive down-regulation of NKX3.1 expression, followed by reduction in mRNA expression of the androdrogen receptor (AR) and the insulinlike growth factor receptor (IGF-1R). Western blot analysis showed strong decreases of NKX3.1, AR, and IGF-1R protein expression. Concomitantly, cell proliferation decreased and expression of prostate-specific antigen (PSA) mRNA and its secretion were diminished, whereas expression of IGF binding protein 3 (IGFBP-3) and MMP tissue inhibitor 3 (TIMP-3) was up-regulated. In tumor cells not deprived of NKX3.1 expression this gene still has a function which might differ from its role in prostate development and carcinogenesis. NKX3.1 knock-down altered the expression of genes highly relevant in prostate cancer cell proliferation and apoptosis. In LNCaP NKX3.1 most probably plays the role of an androgenregulated transcription factor whose down-regulation is paralleled by anti-proliferative and pro-apoptotic effects. Since NKX3.1 can regulate AR expression it may become a target for interference in hormone refractory prostate carcinoma."],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61271"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.rights.access","closedAccess"],["dc.subject","NKX3.1; prostate cancer; tumor suppressor; RNA interference"],["dc.subject.ddc","610"],["dc.title","Functional analysis of NKX3.1 in LNCaP prostate cancer cells by RNA interference"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Kampe, Rovena"],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Koenig, B."],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T09:20:19Z"],["dc.date.available","2018-11-07T09:20:19Z"],["dc.date.issued","2013"],["dc.format.extent","S495"],["dc.identifier.isi","000326843603248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28855"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","European Cancer Congress 2013 - 17th ECCO / 38th ESMO / 32nd ESTRO"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","1879-0852"],["dc.relation.issn","0959-8049"],["dc.title","Blockade of PDGFR family together with SRC leads to diminished proliferation of CRC cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Oberthuer, R."],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T09:20:20Z"],["dc.date.available","2018-11-07T09:20:20Z"],["dc.date.issued","2013"],["dc.format.extent","S494"],["dc.identifier.isi","000326843603244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28856"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","European Cancer Congress 2013 - 17th ECCO / 38th ESMO / 32nd ESTRO"],["dc.relation.eventlocation","Amsterdam, NETHERLANDS"],["dc.relation.issn","1879-0852"],["dc.relation.issn","0959-8049"],["dc.title","Dual blockade of IGF-IR and EGFR sensitizes colorectal cancer cells to 5-FU-based radiochemotherapy in vitro and in vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","821"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","833"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.date.accessioned","2018-11-07T08:31:14Z"],["dc.date.available","2018-11-07T08:31:14Z"],["dc.date.issued","2009"],["dc.description.abstract","Overexpression and activation of tyrosine kinase receptors are common features of colorectal cancer. Using the human colorectal cancer cell lines DLD-1 and Caco-2, we evaluated the role of the insulin-like growth factor-I (IGF-I) receptor (IGF-IR) and epidermal growth factor receptor (EGFR) in cellular functions of these cells. We used the small interfering RNA (siRNA) technology to specifically down-regulate IGF-IR and EGFR expression. Knockdown of IGF-IR and EGFR resulted in inhibition of cell proliferation of DLD-1 and Caco-2 cells. An increased rate of apoptosis was associated with siRNA-mediated silencing of IGF-IR and EGFR as assessed by activation of caspase-3/caspase-7. The combined knockdown of both EGFR and IGF-IR decreased cell proliferation and induced cell apoptosis more effectively than did silencing of either receptor alone. Comparable effects on cell proliferation and apoptosis were observed after single and combinational treatment of cells by the IGF-IR tyrosine kinase inhibitor NVP-AEW541 and/or the EGFR tyrosine kinase inhibitor erlotinib. Combined IGF-IR and EGFR silencing by either siRNAs or tyrosine kinase inhibitors diminished the phosphorylation of downstream signaling pathways AKT and extracellular signal-regulated kinase (ERK)-1/2 more effectively than did the single receptor knockdown. Single IGF-IR knockdown inhibited IGF-1-dependent phosphorylation of AKT but had no effect on IGF-1- or EGF-dependent phosphorylation of ERK1/2, indicating a role of EGFR in ligand-dependent ERK1/2 phosphorylation. The present data show that inhibition of the IGF-IR transduction cascade augments the antipoliferative and proapoptotic effects of EGFR inhibition in colorectal cancer cells. A clinical application of combination therapy targeting both EGFR and IGF-IR could be a promising therapeutic strategy. [Mol Cancer Ther 2009;8(4): 821-33]"],["dc.identifier.doi","10.1158/1535-7163.MCT-09-0058"],["dc.identifier.isi","000265204500013"],["dc.identifier.pmid","19372555"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17079"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1538-8514"],["dc.relation.issn","1535-7163"],["dc.title","Dual silencing of insulin-like growth factor-I receptor and epidermal growth factor receptor in colorectal cancer cells is associated with decreased proliferation and enhanced apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]