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dc.contributor.authorObakan Yerlikaya, Pınar
dc.contributor.authorYıldırım, Şeyma
dc.contributor.authorÖztürk, Mert Burak
dc.contributor.authorBerrak, Özge
dc.contributor.authorÇoker Gürkan, Ajda
dc.contributor.authorArısan, Elif Damla
dc.contributor.authorÜnsal Palavan, Zeynep Narçın
dc.date.accessioned2018-07-17T07:11:50Z
dc.date.available2018-07-17T07:11:50Z
dc.date.issued2015
dc.identifier.issn1300-0152
dc.identifier.other1303-6092
dc.identifier.urihttps://doi.org/10.3906/biy-1501-18
dc.identifier.urihttps://hdl.handle.net/11413/2130
dc.description.abstractThe cyclin-dependent kinase (CDK) inhibitors purvalanol and roscovitine are therapeutic agents that control cell proliferation through regulating cell-cycle machinery. They also affect polyamine (PA) metabolism, which is activated in malignant tissues. Therefore, PA catabolism became a remarkable target in cancer therapies. Induction of the PA catabolic enzyme spermidine/spermine N-1-acetyltransferase (SSAT) is under the control of transcription factors such as NF kappa B and PPAR gamma. The purpose of this study was to investigate the therapeutic potential of CDK inhibitors in combination with PAs in MCF-7 breast cancer cells. In order to understand the involvement of PA catabolic enzyme SSAT in this process we also checked its transcriptional regulation in the presence of CDK inhibitors. MCF-7 cells were exposed to CDK inhibitors in the absence or presence of Spd and Spm. Cell viability loss was evaluated by MTT assay. Apoptosis was determined by annexin-V/PI staining using FACS flow. The SSAT transcription level was measured by qRT-PCR. Intracellular PA pool was determined by HPLC. Protein expressions were assessed by western blotting. We found that CDK inhibitors decreased cell viability in a time-dependent manner and induced apoptosis. Co-treatment of Spd or Spm with CDK inhibitors prevented the apoptotic potential of both drugs. Purvalanol increased SSAT expression levels in a time-dependent manner. Although the induction of SSAT by purvalanol resulted in the activation of NF kappa B at early time points, induction was accomplished by PPAR gamma as a late response after purvalanol treatment. We concluded that both transcriptional control mechanisms could be responsible for SSAT regulation in a time-dependent manner.tr_TR
dc.language.isoen_UStr_TR
dc.publisherTUBİTAK Scientific & Technical Research Council Turkey, Ataturk Bulvarı No 221, Kavaklıdere, Ankara, 00000, Turkeytr_TR
dc.relationTurkish Journal of Biologytr_TR
dc.subjectPolyaminestr_TR
dc.subjectSSATtr_TR
dc.subjectPurvalanoltr_TR
dc.subjectPPAR gammatr_TR
dc.subjectNF kappa Btr_TR
dc.subjectSpermidine/Spermine N-1-Acetyltransferase SSATtr_TR
dc.subjectInduced Apoptosistr_TR
dc.subjectColon-Cancertr_TR
dc.subjectPolyamine Metabolismtr_TR
dc.subjectCarcinoma Cellstr_TR
dc.subjectActivationtr_TR
dc.subjectInductiontr_TR
dc.subjectRoscovitinetr_TR
dc.subjectAutophagytr_TR
dc.subjectAlphatr_TR
dc.titleCDK inhibitors-induced SSAT expression requires NF kappa B and PPAR gamma in MCF-7 breast cancer cellstr_TR
dc.typeArticletr_TR
dc.contributor.authorID156421tr_TR
dc.contributor.authorID125860tr_TR
dc.contributor.authorID113920tr_TR
dc.contributor.authorID6125tr_TR
dc.identifier.wos360285900008
dc.identifier.wos360285900008en


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