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    Association of Clusterin (CLU) Gene Polymorphism, Rs11136000, with Alzheimer's Disease and Diabetes in the Turkish Population
    (Canadian Soc Clinical Investigation, 2015) Ciftci-Yilmaz, Sultan; Oznur, Murat; Ayturk, Zubeyde; Dede, Serap; Cigdem, Sadik; Eroglu, Esra; Onal, Fethi
    Purpose: Alzheimer's disease (AD), the most common form of dementia, is characterized by abnormal protein storage in the brain and primarily causes a progressive loss of memory and all other cognitive functions. According to the World Health Organization (WHO) report, AD is steadily increasing among people 65 years of age and over. Genome wide association studies have shown that various gene polymorphisms are highly associated with the occurrence of AD. Among them, clusterin (CLU) gene polymorphism was identified as one of the highest genetic risks in late-onset AD. Our aim was to investigate the relation of CLU rs11136000 and AD and its potential use as a biomarker for AD susceptibility in the Turkish population. Methods: 50 samples obtained from AD patients and 55 samples obtained from a control group were used for the presented study. Genomic DNA was isolated from peripheral blood by SDS/proteinase K treatment followed by phenol-chloroform extraction and ethanol precipitation. Presence of the CLU rs11136000 polymorphism was investigated by PCR-RFLP and selected samples were confirmed by DNA sequencing. Chi-square test was used for statistical analysis. Results: In the Turkish population, the CLU rs11136000 polymorphism did not show a significant association with AD as compared with the control group (p>0.05). Polymorphic CLU-C allele of AD patients showed an increased association with diabetes (p=0.015) as compared with CLU-T allele of AD patients, whereas in the control group the CLU-C allele did not show a significant association with diabetes (p=0.332). Conclusion: Individuals with diabetes and polymorphic CLU-C allele may have a higher susceptibility to develop AD later in life.
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    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]
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    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]
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    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, Reidar
    BackgroundGenetic 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.
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    Investigation of MACC1 Gene Expression in Head and Neck Cancer and Cancer Stem Cells
    (Canadian Soc Clinical Investigation, 2016) Evran, Ebru; Sahin, Hilal; Akbas, Kubra; Cigdem, Sadik; Gunduz, Esra
    Purpose: By investigating the MACC1 gene (metastasis-associated in colon cancer 1) in cancer stem cells (CSC) resistant to chemotherapy and in cancer stem cells (CSC) resistant to chemotherapy and in cancer cells (CS) sensitive to chemotherapy we determineda steady expression in both types of cells in head and neck cancer. In conformity with the result we examined if this gene could be a competitor gene for chemotherapy. According to literature, the MACC1 gene shows a clear expression in head and neck cancer cells [1]. Here we examined MACC1 expression in CSC and investigated it as a possible biomarker. Methods: Our experiments were performed in the UT -SCC -74 in primary head and neck cancer cell line. We examined the MACC -1 gene expression by Real Time PCR from both isolated CSC and CS. Results: Expression of MACC -1 gene of cancer stem cells showed an two-fold increase compared with cancer cells. Based on the positive expression of MACC1 in both CS and CSC, this gene may serve as a potential biomarker in head and neck cancer. By comparing the results of this study with the novel features of MACC1, two important hypotheses could be examined. The first hypothesis is that MACC1 is a possible transcripton factor in colon cancer, which influences a high expression of CSC in head and neck and affects the expression of three biomarkers of the CSC control group biomarkers. The second hypothesisis is that the positive expression of MACC1 in patients with a malignant prognosis of tongue cancer, which belongs to head and neck cancer types, operates a faster development of CSC to cancer cells.
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    Leukemia-Associated Nup214 Fusion Proteins Disturb the XPO1-Mediated Nuclear-Cytoplasmic Transport Pathway and Thereby the NF-?B Signaling Pathway
    (Amer Soc Microbiology, 2016) Saito, Shoko; Cigdem, Sadik; Okuwaki, Mitsuru; Nagata, Kyosuke
    Nuclear-cytoplasmic transport through nuclear pore complexes is mediated by nuclear transport receptors. Previous reports have suggested that aberrant nuclear-cytoplasmic transport due to mutations or overexpression of nuclear pore complexes and nuclear transport receptors is closely linked to diseases. Nup214, a component of nuclear pore complexes, has been found as chimeric fusion proteins in leukemia. Among various Nup214 fusion proteins, SET-Nup214 and DEK-Nup214 have been shown to be engaged in tumorigenesis, but their oncogenic mechanisms remain unclear. In this study, we examined the functions of the Nup214 fusion proteins by focusing on their effects on nuclear-cytoplasmic transport. We found that SET-Nup214 and DEK-Nup214 interact with exportin-1 (XPO1)/CRM1 and nuclear RNA export factor 1 (NXF1)/TAP, which mediate leucine-rich nuclear export signal (NES)-dependent protein export and mRNA export, respectively. SET-Nup214 and DEK-Nup214 decreased the XPO1-mediated nuclear export of NES proteins such as cyclin B and proteins involved in the NF-kappa B signaling pathway by tethering XPO1 onto nuclear dots where Nup214 fusion proteins are localized. We also demonstrated that SET-Nup214 and DEK-Nup214 expression inhibited NF-kappa B-mediated transcription by abnormal tethering of the complex containing p65 and its inhibitor, I kappa B, in the nucleus. These results suggest that SET-Nup214 and DEK-Nup214 perturb the regulation of gene expression through alteration of the nuclear-cytoplasmic transport system.
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    Suppression of bromodomain-containing protein 4 by shRNA: A new approach for cancer treatment
    (Canadian Soc Clinical Investigation, 2016) Kaya, Turan; Kahraman, Berke; Bazarov, Nurgeldi; Toker, Alperen S.; Celik, Ayse; Cigdem, Sadik; Gunduz, Esra
    Purpose: MYC is a transcription factor coding gene that is believed to control 15% of the genes in the entire human genome. The central role of c-MYC in cancer pathogenesis makes it a major therapeutic target in field of anticancer agent development. Methods: We targeted the acetyl-lysine binding modules or bromodomains, which are associated with c-MYC transcriptional activation. Results: Sequence specific inhibition of BET bromodomains with small hairpin RNAs (shRNAs) resulted in cessation of cellular proliferation in different cancer cell lines. Unlike previous studies on inhibition of bromodomains with selective small-molecule inhibitors, our study revealed the significant role of BET bromodomains in solid tumours and also highlighted the ease of RNA interference (RNAi) methodology for inhibition of bromodomain translation. Conclusion: The degree of influence of BET bromodomain inhibition on proliferation in five cancer cell lines established it as the major target in malignancies characterized by activation of c-MYC.
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    Suppression Of Bromodomaincontaining Protein 4 By Shrna: A New Approach For Cancer Treatment
    (The Canadian Society for Clinical Investigation, 2016) Kaya, Turan; Kahraman, Berke; Bazarov, Nurgeldi; Toker, Alperen S.; Celik, Ayse; Cigdem, Sadik; Gündüz, Esra
    Purpose: MYC is a transcription factor coding gene that is believed to control 15% of the genes in the entire human genome. The central role of c-MYC in cancer pathogenesis makes it a major therapeutic target in field of anticancer agent development. Methods: We targeted the acetyl-lysine binding modules or bromodomains, which are associated with c-MYC transcriptional activation. Results: Sequence specific inhibition of BET bromodomains with small hairpin RNAs (shRNAs) resulted in cessation of cellular proliferation in different cancer cell lines. Unlike previous studies on inhibition of bromodomains with selective small-molecule inhibitors, our study revealed the significant role of BET bromodomains in solid tumours and also highlighted the ease of RNA interference (RNAi) methodology for inhibition of bromodomain translation. Conclusion: The degree of influence of BET bromodomain inhibition on proliferation in five cancer cell lines established it as the major target in malignancies characterized by activation of c-MYC © 2021 Elsevier B.V., All rights reserved.