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Öğe 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.Öğe Cross-regulation of non-coding RNAs and their correlations with target protein-coding genes in CRC pathobiology(Elsevier B.V., 2019) Bozgeyik, Esra; Bozgeyik, İbrahimIlluminating the correlations between non-coding RNAs and protein-coding genes are of great interest to understand more about the molecular mechanisms that drive malignant transformation and understanding such correlations will enable development of more specific and efficient targeted therapeutics. Accordingly, in this comprehensive meta-analysis study, we tried to determine correlations between long non-coding RNA (lncRNA), microRNA (miRNA) and messenger RNA (mRNA) molecules that are involved in the pathogenesis of colorectal cancer (CRC). For the present study, current colorectal cancer studies published until 20 August 2017 and associated with the lncRNA-miRNA-mRNA interactions was included. The current literature search was done online in Pubmed, Embase and Web of Science databases. These databases have been screened with three keywords; “lncRNA” “miRNA” and “colorectal cancer”. As a result, colorectal neoplasia differentially expressed (CRNDE) was determined to be consistently up-regulated in CRC tissues and inversely associated with miR-181a-5p. Also, CRNDE expression was significantly associated with lymph node metastasis (p = 0.032). Additionally, a significant association was determined between CRC and survival time in the OS analysis of FER1L4, TUSC7, UCC and lincRNA-ROR. More importantly, there was a negative correlation between lncRNA-miRNA expressions (p = 0.001). Particularly, CRNDE/miR-181a-5p, FER1L4/miR-106a-5p, TUSC7/miR-211, UCC/miR-143 and lincRNA-ROR/miR-145 was negatively correlated. In addition, there was a significant positive correlation between GAPLINC/CD44 and TUSC7/CDK6 in CRC tissues (p = 0.000). Overall analysis showed that lncRNAs and mRNAs, which are targets of the same miRNA, have positive interactions. In addition, miRNAs were shown to have negative correlations with target lncRNA/mRNA. © 2018 Elsevier B.V.Öğe Enhanced E2F1 activity increases invasive and proliferative activity of breast cancer cells through non-coding RNA CDKN2B-AS1(Elsevier B.V., 2020) Bozgeyik, Esra; Saadat, Khandakar A.S.M.; Arman, K.; Bozgeyik, İbrahim; İkeda, M.A.Long non-coding RNAs have recently appeared as fundamental regulators of gene transcription in several biological processes, but only a few have known functional influences in the malignant transformation of breast cancer. CDKN2B-AS1 gene, also termed ANRIL, encoding a long non-coding RNA is located in the CDKN2B-CDKN2A gene cluster, loss of which is the most frequent alternation in several types of human malignancies. CDKN2B-AS1 is involved in the suppression of tumor suppressor genes (INK4a, ARF, and INK4b) and has been recognized as a direct target of E2F1. However, the roles of E2F1–CDKN2B-AS1 interaction in breast cancer have remained muchly mysterious. In this particular study, we reveal that both CDKN2B and CDKN2B-AS1 genes were differentially expressed in breast cancer cells in contrast to breast epithelial cells. Ectopic expression of E2F1 activated CDKN2B-AS1 but not CDKN2B expression. Lastly, overexpression of E2F1 improved the colony formation and migratory capacities of breast cancer cells. These results suggest that enhanced E2F1 activity increased invasive and proliferative activity of breast cancer but not breast epithelial cells possibly through up-regulating CDKN2B-AS1 transcript. © 2020 Elsevier B.V.Öğe MIRNA-mediated regulation of the PI3K/AKT signaling pathway in colorectal cancer: A study based on data mining(2019) Bozgeyik, Esra; Bozgeyik, İbrahimAim: In colorectal cancer (CRC), expression of genes involved in the PI3K/Akt signaling pathway varies significantly. Studies haveshown that microRNAs (miRNA) have important roles in the development of CRC. Accordingly, the aim of this study was to determinemiRNAs affecting the critical genes in the PI3K/Akt pathway by analysis of The Cancer Genome Atlas (TCGA) CRC data sets and toevaluate the clinical significance of these miRNAs.Material and Methods: Initially, CRC mRNA, miRNA expression levels and patient data were obtained from TCGA database. The studyincluded 220 CRC patients. MiRNAs that were negatively correlated with genes in the PI3K/Akt signaling pathway were selected, andtheir expression levels were compared with the clinical and demographic characteristics of CRC patients.Results: miR-18a, miR-19b, miR-17, miR-106b, miR-130b and miR-135b were found to be negatively correlated with genes that playkey roles in the PI3K/Akt pathway. Also, miR-18a, miR-19b, miR-17 and miR-135b were found to vary significantly according to theCRC subtype.Conclusion: Consequently, the PI3K/Akt signaling pathway was found to be deregulated in CRC and the majority of genes involved inthis signaling pathway were associated with miRNAs. Thus, PI3K/Akt miRNA axis might serve as a potentially distinctive diagnostic,prognostic and therapeutic avenue against CRC.Öğe 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 AliThiosemicarbazones (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.Öğe Novel zinc oxide nanoparticles of Teucrium polium suppress the malignant progression of gastric cancer cells through modulating apoptotic signaling pathways and epithelial to mesenchymal transition(Elsevier, 2023) Bozgeyik, İbrahim; Ege, Miray; Temiz, Ebru; Erdal, Berna; Koyuncu, İsmail; Temiz, Cengiz; Bozgeyik, EsraManagement of gastric cancer is still challenging due to resistance to current chemotherapeutics and recurrent disease. Moreover, green-synthesized zinc oxide nanoparticles (ZnO-NPs) using natural resources are one of the most promising therapeutic agents for anticancer therapy. Here we report the facile green synthesis and char-acterization of ZnO-NPs from Teucrium polium (TP-ZnO-NP) herb extract and the anticancer activities of these nanoparticles on gastric cancer cells. Facile green synthesis of TP-ZnO-NP was achieved using zinc acetate dihydrate. For the characterization of TP-ZnO-NP, UV-vis spectroscopy, FTIR, SEM, XRD and EDX analyses were performed. Antiproliferative and anticancer activities of TP-ZnO-NP were explored using the HGC-27 gastric cancer cell line model. MTT cell viability and colony formation assays were used for the analysis of cell pro-liferation and migration. Wound healing assay was used to analyze the migration capacities of cells. Annexin V/ PI double staining, DNA ladder assay, and Acridine orange/Ethidium bromide staining were performed to analyze the induction of apoptosis. qPCR was used to determine gene expression levels of apoptotic and epithelial to mesenchymal transition marker genes. The aqueous extract of TP served as both a reducing and capping agent for the successful biosynthesis of zinc oxide nanoparticles. Remarkably, synthesized TP-ZnO-NPs were found to have significant antiproliferative and anticancer activities on HGC-27 gastric cancer cells. Collectively, current data suggest that TP-ZnO-NP is a novel and promising anticancer agent for future therapeutic interventions in gastric cancer.Öğe The Role and Antagonistic Effects of miR-16-5p in the Regulation of ADP-Ribosylation Factor-Like Tumor Suppressor Gene 1 in Lung Cancer Cells(2023) Yüksel, Tuğba Nurcan; Bozgeyik, Esra; Bozgeyik, İbrahimObjective: ADP-ribosylation factor-like tumor suppressor gene 1 is a member of the Ras superfamily of small guanosine triphosphatases that are known to be involved in multiple regulatory pathways in the multistage development of human cancers. Also, ADP-ribosylation factor-like tumor suppressor gene 1 expression levels have been reported to be dramatically lower in both cancer cell lines and tumor tissues compared to con- trols. Accordingly, defects in the regulation of the ADP-ribosylation factor-like tumor suppressor gene 1 gene seems have key tumor suppressive effects in the formation and development of human cancers including lung cancer. Moreover, microRNAs regulating the expression of ADP-ribosylation factor-like tumor suppressor gene 1 have not been described previously. Accordingly, the present study aimed to reveal the influence of miR-16-5p on the regulation of ADP-ribosylation factor-like tumor suppressor gene 1 gene. Materials and Methods: A549 lung adenocarcinoma cells were used. For the overexpression and silencing experiments of miR-16-5p synthetic microRNA mimics and inhibitors were used, respectively. Gene expres- sion analyses were achieved with the help of quantitative real-time polymerase chain reaction. Results: MiR-16-5p was identified to be predictive target of ADP-ribosylation factor-like tumor suppressor gene 1 and directly targets the expression of ADP-ribosylation factor-like tumor suppressor gene 1 as revealed by the overexpression and silencing experiments. Specifically, it was found that miR-1 6-5p-overexpressed A549 cells showed a decrease in ADP-ribosylation factor-like tumor suppressor gene 1 gene expression, whereas miR- 16-5p-suppressed cells showed an increase in expression. These findings possibly suggest that miR-16-5p is the direct regulatory microRNA that posttranscriptionally regulates the expression of ADP-ribosylation factor-like tumor suppressor gene 1. Conclusion: Collectively, miR-16-5p seems to be a key regulatory molecule involved in the posttranscrip- tional regulation of the ADP-ribosylation factor-like tumor suppressor gene 1, and it might be responsible for the downregulation of this gene in lung cancer.Öğe Uzun Kodlamayan RNA NORAD’ın Mitomisin C İlişkili Kemorezistansta Olası Rolü(2022) Bozgeyik, İbrahimAmaç: Non-coding RNA activated by DNA damage (NORAD), deoksiribo nükleik asit (DNA) hasarı cevabı sırasında aktive olan bir uzun kodlamayan ribonükleik asittir (RNA). Çalışmalar, NORAD’ın insan kanserlerinde aşırı eksprese edildiğini ve ilaca bağlı kemorezistans ile ilişkili olduğunu göstermektedir. Bu çalışma, mitomisin C ile ilişkili kemorezistans ve mitomisin C ile indüklenen DNA hasar yanıtı sırasında spesifik olarak aktive edilen bir uzun kodlamayan RNA NORAD’ın olası rolünü araştırmayı amaçlamaktadır. Gereç ve Yöntem: Hücre kültürü deneylerinde MDA-MB-231 meme kanseri hücreleri kullanıldı. Mitomisin C’nin meme kanseri hücreleri üzerindeki etkilerini belirlemek için MTT hücre canlılığı testi kullanıldı ve uygulama dozu buna göre belirlendi. NORAD gen ekspresyon düzeylerinin analizi için kantitatif qPCR yöntemi kullanıldı. Bulgular: Mitomisin C’nin meme kanseri hücrelerinin hücre canlılığını doza bağlı olarak baskıladığı ve yarı-maksimum inhibisyon konsantrasyonunun 1,12 µg/mL olduğu belirlendi (p<0,0001). Özellikle, mitomisin C ile muamele edilen meme kanseri hücrelerinde NORAD’ın önemli bir farklı aktivasyonu belirlendi (p<0,0001). Sonuç: Burada elde edilen bulgular, mitomisin C ile ilişkili kemoresistans ve mitomisin C ile indüklenen DNA hasar yanıtında NORAD’ın olası rolünün olabileceğini göstermektedir.
