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dc.contributor.authorErbaykent Tepedelen, Burcu
dc.contributor.authorÖzmen, Besra
dc.contributor.authorVarışlı, Lokman
dc.contributor.authorGönen Korkmaz, Ceren
dc.contributor.authorDebeleç Bütüner, Bilge
dc.contributor.authorHamid, Syed Muhammad
dc.contributor.authorÇakmak, Özgür Yılmazer
dc.contributor.authorKorkmaz, Kemal Sami
dc.date.accessioned2017-03-01T12:09:04Z
dc.date.available2017-03-01T12:09:04Z
dc.date.issued2011-10
dc.identifier.citationErbaykent-Tepedelen, B., Özmen, B., Varışlı, L., Gönen-Korkmaz, C., Debeleç-Bütüner, B., Hamid, S. M., Çakmak, Ö. Y., and Korkmaz, K. S. (2011). NKX3.1 contributes to S phase entry and regulates DNA damage response (DDR) in prostate cancer cell lines. Biochemical and Biophysical Research Communications, 414(1), 123-128. doi:10.1016/j.bbrc.2011.09.035en_US
dc.identifier.issn0006-291X
dc.identifier.urihttp://doi.org/10.1016/j.bbrc.2011.09.035
dc.identifier.urihttp://hdl.handle.net/11147/4938
dc.description.abstractNKX3.1 is an androgen-regulated homeobox gene that encodes a tissue-restricted transcription factor, which plays an important role in the differentiation of the prostate epithelium. Thus, the role of NKX3.1 as a functional topoisomerase I activity enhancer in cell cycle regulation and the DNA damage response (DDR) was explored in prostate cancer cell lines. As an early response to DNA damage following CPT-11 treatment, we found that there was an increase in the γH2AX (S139) foci number and that total phosphorylation levels were reduced in PC-3 cells following ectopic NKX3.1 expression as well as in LNCaP cells following androgen administration. Furthermore, upon drug treatment, the increase in ATM (S1981) phosphorylation was reduced in the presence of NKX3.1 expression, whereas DNA-PKcs expression was increased. Additionally, phosphorylation of CHK2 (T68) and NBS1 (S343) was abrogated by ectopic NKX3.1 expression, compared with the increasing levels in control PC-3 cells in a time-course experiment. Finally, NKX3.1 expression maintained a high cyclin D1 expression level regardless of drug treatment, while total γH2AX (S139) phosphorylation remained depleted in PC-3, as well as in LNCaP, cells. Thus, we suggest that androgen regulated NKX3.1 maintains an active DDR at the intra S progression and contributes to the chemotherapeutic resistance of prostate cancer cells to DNA damaging compounds.en_US
dc.description.sponsorshipTUBITAK-106S200, -110S134, COST action BM0703 CANGENIN (TUBITAK -108S288); Turkish Scientific and Technological Research Council and BAP projects (06MUH004 and 10MUH006)en_US
dc.language.isoengen_US
dc.publisherAcademic Press Inc.en_US
dc.relation.isversionof10.1016/j.bbrc.2011.09.035en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNKX3.1en_US
dc.subjectPATM (S1981)en_US
dc.subjectProstate canceren_US
dc.subjectTopoisomerase inhibitor CPT-11en_US
dc.subjectDNA damage responseen_US
dc.subjectγH2AX (S139) focien_US
dc.titleNKX3.1 contributes to S phase entry and regulates DNA damage response (DDR) in prostate cancer cell linesen_US
dc.typearticleen_US
dc.contributor.institutionauthorÇakmak, Özgür Yılmazer
dc.relation.journalBiochemical and Biophysical Research Communicationsen_US
dc.contributor.departmentIzmir Institute of Technology. Biotechnology and Bioengineering Research and Application Center (IZTECH BIYOMER)en_US
dc.identifier.volume414en_US
dc.identifier.issue1en_US
dc.identifier.startpage123en_US
dc.identifier.endpage128en_US
dc.identifier.wosWOS:000296215200023
dc.identifier.scopusSCOPUS:2-s2.0-80054070288
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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