Fen Edebiyat Fakültesi / Faculty of Letters and Science

Permanent URI for this collectionhttps://hdl.handle.net/11727/1396

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2014 - 20152

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Author: search.filters.author.Terzi, Yunus Kasimsearch.filters.applied.f.language: search.filters.language.eng

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    beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration
    (2014) Iseri, Ozlem Darcansoy; Sahin, Feride Iffet; Terzi, Yunus Kasim; Yurtcu, Erkan; Erdem, S. Remzi; Sarialioglu, Faik; 25026350
    Context: Propranolol, atenolol, and ICI118,551 are non-selective beta-adrenergic receptor (AR), beta(1)-AR, and beta(2)-AR antagonists, respectively. Objective: We investigated the efficacy of propranolol, atenolol, and ICI118,551 on proliferation, migration, and invasion of non-stimulated breast (MCF7), colon (HT-29), and hepatocellular (HepG2) cancer cells. Materials and methods: beta-AR expression profiling of cells was performed by real time PCR. Cell proliferation was determined by MTT. Boyden chamber and scratch assays were performed to evaluate invasion and migration. Results and discussion: All cell lines expressed beta-ARs. ICI118,551 was the most cytotoxic, whereas atenolol was the least effective beta-AR antagonist for 24, 48, and 72 h. Cell invasion was inhibited by ICI118,551 (45, 46, and 50% for MCF7, HT29, and HepG2, respectively) and propranolol (72, 65, and 90% for MCF7, HT29, and HepG2, respectively). Propranolol, atenolol, and ICI118,551 reduced migration of MCF7, HT-29, and HepG2 cells to varying extents depending on the application concentration and duration. Propranolol and atenolol reduced migration of MCF7 and HT-29 in a concentration-dependent manner, whereas migration of these cells decreased after 48 and 72 h of ICI118,551 applications. Conclusion: Beta(2)-AR antagonist seemed to be the most cytotoxic beta-blocker on non-stimulated cancer cells. Propranolol and ICI118,551 were more effective than atenolol in inhibiting invasion and migration of non-stimulated MCF7 and HT-29 cells; ICI118,551 being the most potent. Concordantly, beta(2)-selective blockage seemed to be more effective for non-stimulated cells. Effect of the selective beta-AR antagonists showed variation depending on the concentration, incubation time, and histological origin of cells.
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    Epigallocatechin 3-gallate applications on HT-29 and MCF-7 cell lines and evaluation of tumor suppressor gene methylation
    (2015) Terzi, Yunus Kasim; Kaya, Ozge Ozer; Iseri, Ozlem Darcansoy; Celik, Zerrin; Sahin, Feride Iffet
    Epigallocatechin 3-gallate (EGCG) is an antitumor molecule and shows this activity by binding to the active center of a methyltransferase enzyme (DNMT1). The methylation of DNA sequences of tumor suppressor and DNA repair genes is observed in different stages of carcinogenesis. In this study, we analyzed the effect of EGCG on the methylation status of 25 tumor suppressor genes in cancer cell lines HT-29 and MCF-7. HT-29 and MCF-7 cells were incubated with 10 mu M, 20 mu M, and 50 mu M and 1 mu M, 5 mu M, and 10 mu M EGCG for 48 h, respectively. We found promoter hypermethylation of (1) CDH13, GATA5, and RAR beta genes in MCF-7 cell line and (2) RAR beta, ESR1, PAX6, WT1, CADM1, CHFR, CDH13, and GATA5 genes in HT-29 cell line. However, (3) after EGCG application, no changes in methylation status were detected in our samples. Our results suggest that methylation status of tumor suppressor genes did not change with different EGCG doses.