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Öğe Boric acid inhibits cell proliferation through RB1 protein in head and neck cancer(Amer Assoc Cancer Research, 2015) Gunduz, Esra; Hatipoglu, Omer Faruk; Cigdem, Sadik; Erdogan, Kubra; Elitok, Mustafa Semih; Grenman, Reidar; Erdamar, Husamettin[Abstract Not Available]Öğe Characterization of cancer stem cell properties and identification of invasion as well as metastatic process in head and neck cancer(Amer Assoc Cancer Research, 2015) Gunduz, Mehmet; Hatipoglu, Omer Faruk; Gunduz, Esra; Cetin, Elif Nihan; Uctepe, Eyyup; Cigdem, Sadik; Grenman, Reidar[Abstract Not Available]Öğe Functional analysis of ESM1 by siRNA knockdown in primary and metastatic head and neck cancer cells(Wiley, 2018) Bender, Onur; Gunduz, Mehmet; Cigdem, Sadik; Hatipoglu, Omer Faruk; Acar, Muradiye; Kaya, Mesut; Grenman, ReidarBackgroundGenetic factors play a large role in cancer, and thus, there is a great desire to understand the effects of different genes in cancer and to also develop gene therapy for better treatments. Therefore, the development of alternative diagnosis and therapy modalities is of utmost importance. The aim of our study was to illuminate the role of ESM1 (endothelial cell-specific molecule-1, also known as Endocan) in proliferation and migration of head and neck cancer, thus helping to pave the way for new treatment modalities and predictive biomarkers. MethodsESM1 expression was shown with immunofluorescence assay using confocal laser scanning microscope in primary and metastatic head and neck cancer cells. ESM1 expression was knocked down by RNA interference in head and neck cancer cells. Knockdown efficiency was evaluated by quantitative real-time RT-PCR and Western blot. Cell proliferation and migration assays were performed by xCELLigence real-time cell analysis system. ResultsImmunofluorescence assay showed nuclear localization and high expression of ESM1 in primary and metastatic head and neck cancer cells. ESM1 mRNA and protein levels were significantly decreased in ESM1-knockdown cells compared to control. ESM1-knockdown cells showed reduced proliferation and migration activity when compared to control cells. ConclusionThese findings suggest that ESM1 has roles on proliferation and migration of head and neck cancer cells.Öğe Leptin induces ADAMTS-4, ADAMTS-5, and ADAMTS-9 genes expression by mitogen-activated protein kinases and NF-?B signaling pathways in human chondrocytes(Wiley, 2015) Yaykasli, Kursat Oguz; Hatipoglu, Omer Faruk; Yaykasli, Emine; Yildirim, Kubra; Kaya, Ertugrul; Ozsahin, Mustafa; Uslu, MustafaElucidation of the causes of inflammation has vital importance in the development of new approaches for the treatment of arthritic diseases. The degradation of aggrecan by upregulated disintegrin and metalloproteinase with trombospondin motifs (ADAMTSs) is the key event in the development of both rheumatoid arthritis (RA) and osteoarthritis (OA). Increased levels of leptin in both RA and OA have been demonstrated, thus linking leptin to arthritic diseases, but the mechanism has not been clarified. This study investigated the putative role of signaling pathways (p38, JNK, MEK1, NF-?B, and PI3) involved in leptin-induced cartilage destruction. Normal human articular chondrocytes were cultured with recombinant human leptin at 100, 250, 500, and 1000ng/mL doses for 6, 12, 24, and 48h, after which ADAMTS-4, -5, and -9 genes expression were determined by real time-polymerase chain reaction (RT-PCR) and Western Blot methods. The signaling pathways involved in leptin-induced ADAMTSs upregulation were also investigated by using inhibitors of signaling pathways. It was demonstrated that ADAMTSs expression level was peaked at 1000ng/mL doses for 48hours, and MAPKs (p38, JNK, and MEK) and NF-?B signaling pathways involving in leptin triggered ADAMTSs upregulation. Obesity as a risk for RA and OA may contribute to the inflammation of both RA and OA diseases by secreting adipokines like leptin. We hypothesize that leptin is involved in the development of RA and OA accompanied with obesity by increasing ADAMTS-4, -5, and -9 genes expression via MAPKs and NF-?B signaling pathways.Öğe Matrix Metalloproteinases 2 and 9 Polymorphism in Patients With Myeloproliferative Diseases A STROBE-Compliant Observational Study(Lippincott Williams & Wilkins, 2015) Maral, Senem; Acar, Muradiye; Balcik, Ozlem Sahin; Uctepe, Eyyup; Hatipoglu, Omer Faruk; Akdeniz, Derya; Altun, Hatice UludagChronic myeloproliferative disorders such as polycythemia vera (PV), essential thrombocytosis (ET), and idiopathic myelofibrosis arise from clonal proliferation of neoplastic stem cells in the bone marrow. Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that have potential to degrade all types of extracellular matrix (ECM) and also play a role in remodeling of the ECM. It is known that MMPs play a role in bone marrow remodeling. The primary goal of our study is to explore the relationship between chronic myeloproliferative diseases and some of MMP gene polymorphisms. The demonstration of a relationship will help to understand whether these polymorphisms may be a potential early diagnosis marker of the diseases. Patients were selected from outpatient clinks of Turgut Ozal University Hospital, Ankara, Turkey, between December 2010 and May 2011. Twenty-eight patients that previously diagnosed and followed-up with PV, 17 with secondary polycythemia (SP), and 12 with ET were enrolled in the study, along with a control group of 22 healthy people. DNA was isolated from peripheral blood. Using polymerase chain reaction restriction fragment length polymorphism method, MMP2 and MMP9 gene polymorphisms were analyzed with agarose gel electrophoresis. There was a statistically significant difference between the study groups and the control group in terms of Gin279Arg polymoiphisms rates of MMP9. The highest MMP9 Gln279Arg polymorphism rate was observed in the ET group. But nobody from the control group had polymorphic MMP9. There was no statistically significant difference between the groups in terms of MMP2-735 C > T polymorphism rates. In conclusion, MMP9 gene Gln279Arg polymorphism was associated with ET, SP, and PV diseases. Hence, we believe that these gene polymorphisms may play a role in the mechanism of bone marrow fibrosis and may be a factor that increases the risk of thrombosis. Illumination of the molecular basis of the relationship between MMP-thrombosis and MMP-librosis provides a better understanding of the pathophysiology of PV and ET diseases mid will allow new approaches to diagnosis and treatment.Öğe Potential genetic biomarkers in the early diagnosis of Alzheimer disease: APOE and BIN1(Tubitak Scientific & Technological Research Council Turkey, 2015) Kaya, Gulhan; Gunduz, Esra; Acar, Muradiye; Hatipoglu, Omer Faruk; Acar, Burcu; Ilhan, Atilla; Gunduz, MehmetBackground/aim: Alzheimer disease (AD) is triggered by interactions of multiple genetic and environmental factors. The APOE gene E4 allele is the best-known risk factor for AD, yet it represents a small ratio of genetic factors. According to genome-wide association studies, the BIN1 gene is the second important risk factor for AD, following the APOE gene. We aimed to identify a novel biomarker indicating susceptibility to AD by investigating APOE alleles and BIN1 gene polymorphisms in a Turkish population. Materials and methods: Fifty-three AD patients and 56 controls were included to examine polymorphism and allele frequency of the APOE and BIN1 genes. Genomic DNAs were isolated from whole blood by SDS/proteinase K treatment, phenol-chloroform extraction, and ethanol precipitation. RFLP was done for identification of polymorphisms in the APOE gene and allele-specific PCR was used for the BIN1 gene. Results: Frequency of the APOE E4 allele was higher in the AD patient group, while the frequency of the E2 allele was higher in controls. The E4/E4 genotype was detected in the AD patient group, while this genotype was not observed in the controls. The frequencies of BIN1 alleles were similar in both groups. Conclusion: There was a strong association between AD and the APOE E4 allele, while no such relation was observed with BIN1 gene polymorphism.Öğe The effects of hypericin on ADAMTS and p53 gene expression in MCF-7 breast cancer cells(Imprimatur Publications, 2014) Acar, Muradiye; Ocak, Zeynep; Erdogan, Kubra; Cetin, Elif Nihan; Hatipoglu, Omer Faruk; Uyeturk, Ummugul; Gunduz, EsraPurpose: The purpose of this study was to determine the effects of hypericin on MCF-7 (Michigan Cancer Foundation-7) breast cancer cells, as it is known to exert an antitumor effect on the expression and regulation of ADAMTS1, 3, 10 and the p53 gene in breast cancer cells. Methods: MFC-7 cells were cultured and subjected separately to various doses (1, 5 and 7.5 mu g/mL) hypericin. After 24 hrs, RNA was isolated and transcribed into cDNA. Expression analysis was performed by real time (RT)-PCR and cell survival was determined by the XTT assay. Results: While the expression of ADAMTS1 in MFC-7 cells decreased to 0.04-fold after exposure to 1 mu g/mL hypericin, the expression increased by 5.6- and 36-fold with 5 and 7.5 mu g/mL, respectively. Furthermore, ADAMTS3 expression in MCF7 cells increased 3.9-fold with the use of 5 mu g/mL of hypericin. These concentrations of hypericin did not lead to significant changes in the expression of ADAMTS10 and the p53 gene. Viability of cancer cells as evaluated by the XTT assay showed that hypericin concentration of 7.5 mu g/mL led to increased apoptosis of cancer cells. Conclusion: The increase in ADAMTS1 expression may prevent metastasis or facilitate the development of an adjuvant factor with tumor-suppressive effects. Hypericin may therefore exert its antitumor and apoptotic effects in MFC-7 cells via ADAMTS1 and ADAMTS3.
