Yazar "Grenman, Reidar" seçeneğine göre listele

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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 the expression of RIF1 gene on head and neck, pancreatic and brain cancer and cancer stem cells
    (Canadian Soc Clinical Investigation, 2016) Cila, Hacer E. Gurses; Acar, Muradiye; Barut, Furkan B.; Gunduz, Mehmet; Grenman, Reidar; Gunduz, Esra
    Purpose: Recent studies have shown that cancer stem cells are resistant to chemotherapy. The aim of this study was to compare RIF1 gene expression in head and neck, pancreatic cancer and glioma cell lines and the cancer stem cells isolated from these cell lines. Methods: UT-SCC-74 from Turku University and UT-SCC-74B primary tumor metastasis and neck cancer cell lines, YKG-1 glioma cancer cell line from RIKEN, pancreatic cancer cell lines and ASPC-1 cells from ATCC were grown in cell culture. To isolate cancer stem cells, ALDH-1 for UT-SCC-74 and UT-SCC-74B cell line, CD-133 for YKG-1 cell line and CD-24 for ASPC-1 cell line, were used as markers of cancer stem cells. RNA isolation was performed for both cancer lines and cancer stem cells. RNAs were converted to cDNA. RIF1 gene expression was performed by qRT-PCR analysis. RIF1 gene expression was compared with cancer cell lines and cancer stem cells isolated from these cell lines. The possible effect of RIF1 gene was evaluated. Results: In the pancreatic cells, RIF1 gene expression in the stem cell-positive cell line was 256 time that seen in the stem cell-negative cell line. Conclusion: Considering the importance of RIF1 in NHEJ and of NHEJ in pancreatic cancer, RIF1 may be one of the genes that plays an important role in the diagnoses and therapeutic treatment of pancreatic cancer. The results of head and neck and brain cancers are inconclusive and further studies are required to elucidate the connection between RIF1 gene and these other types of cancers.
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    Role of miR-200c/miR-141 in the regulation of epithelial-mesenchymal transition and migration in head and neck squamous cell carcinoma
    (Spandidos Publ Ltd, 2014) Tamagawa, Shunji; Beder, Levent Bekir; Hotomi, Muneki; Gunduz, Mehmet; Yata, Kazuya; Grenman, Reidar; Yamanaka, Noboru
    Epithelial-mesenchymal-transition (EMT) is a critical step in tumor invasion and metastasis, while its fate is mainly defined by the balanced expression between the miR-200 family and ZEB transcription factors. In this study, we observed a reciprocal correlation between miR-200c/mir-141 and ZEB1, as well as between ZEB2 and E-cadherin expression in a panel of 13 head and neck squamous cell carcinoma (HNSCC) cell lines. We also confirmed that the enforced expression of miR-200c and miR-141 significantly reduced the migration capacity of HNSCC cells. Accordingly, the enforced expression of miR-200c and mir-141 resulted in a significant upregulation in E-cadherin expression, contrary to the significant downregulation in ZEB1 expression in 3 cell lines (UTSCC-24A, UTSCC-24B and UTSCC-6A cells). Another pair of cell lines, UTSCC-60A and UTSCC- 60B failed to show a significant change in the expression of E-cadherin or ZEB1/ZEB2 during the enforced expression of miR-200c/miR-141. To address the issue, we focused on the hypermethylation status of the ZEB1/2 promoters, which have both been shown to include wide CpG islands. We observed a marked upregulation in both ZEB1 and ZEB2 mRNA expression following treatment with a demethylating agent in both pairs of UTSCC cell lines. In conclusion, our findings confirm the existence of a reciprocal correlation between the mir-200 family and the ZEB family, and demonstrate the role of the miR-200 family in EMT, as well as in the migration and invasion ability of HNSCC cells. Furthermore, our data suggest that the promoter hypermethylation of ZEB1 and ZEB2 may play an essential role and may overshadow the effects of the miR-200 family in the regulation of EMT during carcinogenesis.