Fen Edebiyat Fakültesi / Faculty of Letters and Science

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

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End date: 2019Subject: search.filters.subject.HT-29

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    Assessment of the effects of radiofrequency radiation on human colon epithelium cells
    (2019) Tomruk, A.; Terzi, Y.K.; Guler, Ozturk G.; 0000-0001-5612-9696; 31023054; B-4372-2018
    OBJECTIVES: The aim of the study was to investigate the possible effects of radiofrequency radiation (RFR) at different frequencies for different exposure durations on caspase-dependent apoptosis pathways in human colon adenocarcinoma (HT-29). METHODS: HT-29 cells were exposed to 1800 MHz; 2100 MHz and 2600 MHz RFR for 3 h cont., 6 h int. and 6 h cont.. Cell viability measurements were performed by Trypan Blue exclusion assay and the gene expressions of CASP8, CASP9, CASP3 and CASP12 were analyzed using qRT-PCR. RESULTS: Exposure to 2100 MHz RFR for all 3 durations of exposures was more effective for the ratio of the number of viable HT-29 cells w.r.t 1800 MHz RFR and 2600 MHz RFR exposures. After 2100 MHz RFR exposure, caspase activation increased significantly (for 3h cont. and 6 h int. exposures CASP8 and CASP9 levels; for 6 h cont. exposure CASP3 levels) (p < 0.05). Exposures to both 1800 MHz and 2600 MHz RFR for 3 different exposure durations did not change the activation of caspases we analyzed in this study (p > 0.05). CONCLUSION: Decreases in the cell viability of HT-29 cells for certain frequencies and also durations are consistent with signifi cant increases in caspase activations. The results of caspase activation after 1800 MHz or 2600 MHz RFR exposures can be interpreted as the activation of different types of cell death pathway by caspase signaling cascades (Fig. 15, Ref. 56).
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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.