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    ARID3A-mediated modulation of TP73 and TP73-AS1 in osteosarcoma cells
    (Elsevier Inc, 2020) Saadat, Khandakar A.S.M.; Bozgeyik, Esra; Arman, Kaifee; Bozgeyik, İbrahim; İkeda, M.A.
    Osteosarcoma is the most common primary malignancy arising from bone. Increasing mass of indications suggest that long non-coding RNAs (lncRNAs) play crucial roles in the development of progressions of human cancers including osteosarcoma. Although several lncRNAs have shown to be involved in the molecular pathogenesis of osteosarcoma, identification of novel lncRNAs involved in the osteosarcoma pathobiology remained muchly elusive. Besides, ARID3A is a member of ARID family of DNA binding proteins. ARID3A was also implicated in osteosarcoma pathogenesis. Accordingly, in the present study, we mechanistically investigated the effect of ARID3A on the expression of TP73 and TP73-AS1 in osteosarcoma cells and to determine the relationship between them. For the overexpression of ARID3A in U2-OS cells, pER_xpress_ARID3A expression vector and for the silencing of ARID3A, ARID3A-spesific siRNA was used. Expression levels of ARID3A, TP73 and TP73-AS1 genes were determined by qPCR method. As a result, expression levels of TP73-AS1 were well-correlated with the ARID3A expression levels whereas TP73 expression levels were not well-correlated with ARID3A. In conclusion, our results indicate that ARID3A might be involved in the regulation of TP73-AS1 in osteosarcoma. To our knowledge, this is the first study revealing the role of ARID3A in the regulation of TP73 and TP73-AS1 genes. © 2020 Elsevier Inc.
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    Novel thiosemicarbazone derivative 17B interferes with the cell cycle progression and induce apoptosis through modulating downstream signaling pathways
    (Elsevier, 2020) Bozgeyik, Esra; Taşdemir Kahraman, Demet; Arman, Kaifee; Bozgeyik, İbrahim; Karaküçük İyidoğan, Ayşegül; Çakmak, Ecir Ali
    Thiosemicarbazones (TSCs) are interesting group of chemical compounds that received significant levels of attention due their wide range of pharmacological effects including antibacterial, antiviral, and especially anti-tumor activities. Several thiosemicarbazone derivatives have been extensively reported recently with their anti-tumor properties but designing and developing novel thiosemicarbazone derivatives with more potent chemotherapeutic activities is of great interest for cancer future cancer therapy. Thus, here we aimed to demonstrate as yet undetermined anti-cancer properties of novel thiosemicarbazone derivative 17B. Viability of cells was determined using MTT assay and LDH activities were analyzed using lactate dehydrogenase activity assay. Apoptosis were assayed using Annexin V-FITC and PI double staining method and cell cycle analysis was achieved by using PI staining with fluorescence-activated cell sorting and migration capacities of cells were determined by wound healing assay. As a result, 17B limited cell viability and showed cytotoxic effects in a dose-dependent manner in A549, MCF7 and U2OS cells. In addition, it inhibited progression through cell cycle by interfering with the Gl/S transition and triggered apoptosis by modulating expression levels of pro-apoptotic and anti-apoptotic mediators in MCF7 and U2OS cells. Also, 17B significantly impaired the migration of cancer cells and delayed wound healing in all cells. Consequently, findings of the present study have strongly indicated that 17B might be a novel anti-cancer agent for the treatment of breast cancer and osteosarcoma but not for lung cancer. Our results have provided mechanistic insights into anti-cancer properties of a novel thiosemicarbazone derivative 17B.