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Yayın Effects of leptin on the viability of MCF-7 and T47D cells at different glucose concentrations(Ondokuz Mayis Universitesi, 2020) Demirel, P.B.; Dogan, S.; Ozorhan, U.; Tuna, B.G.; Schuster, T.F.; Cleary, M.P.Obesity is associated with increased risk of breast cancer. Leptin is a well-known factor involved in obesity and its serum levels are increased in breast cancer. Hyperglycemia is another significant risk factor for breast cancer. Consistently, high glucose induces proliferation and invasion of breast cancer cells and in-vivo calorie restriction reduce tumorigenesis in rodent models. The aim of this study was to investigate the effect of leptin on the viability and mode of cell death in breast cancer cells incubated in different glucose concentrations to represent caloric restriction. For this purpose, MCF-7 and T47D breast cancer cells incubated in different glucose concentrations for a total of 72 hours were treated with or without leptin either for one hour or 24 hours and the ratio of apoptotic, necrotic and alive cells were analyzed by flow cytometry. Our data revealed that glucose incubation significantly decreased apoptosis and necrosis, while increasing viability in both cell lines in a dose dependent manner. One-hour leptin treatment significantly decreased viability, and increased apoptosis but did not significantly affect necrosis in T47D cells incubated in 2.5 mM glucose. In MCF-7 cells, one-hour leptin incubation significantly increased necrosis but its effects on apoptosis and viability were not significant. In conclusion, although glucose induces cell death by apoptosis and necrosis in T47D and MCF-7 cells respectively in a dose dependent manner, the overallviability is still increased in both cell lines. One-hour leptin treatment reverses the effect of low glucose incubation on apoptosis of T47D and necrosis of MCF-7 cells. Moreover, the effect of one-hour leptin treatment on apoptosis or necrosis is significantly higher than that of 24-hour leptin treatment. © 2020 Ondokuz Mayis Universitesi. All rights reserved.Yayın LEPTIN RECEPTORS EXPRESSION IN MAMMARY TUMORS AND MAMMARY FAT PAD OF TRANSGENIC MAMMARY CANCER MOUSE MODEL(Morion LLC, 2022) Yılmaz, E.; Thomas, P.B.; Tuna, B.G.; Cleary, M.P.; Dogan, S.Background: Leptin is an adipokine encoded by the Ob (obese) gene and predominantly produced by adipocytes. The roles of both leptin and leptin receptor (ObR) in numerous pathophysiological conditions including mammary tumor (MT) development have been reported. Aim: To examine protein expression levels of leptin and its receptors (ObR) including the long form, ObRb, in MT tissue and mammary fat pad of a transgenic mammary cancer mouse model. Further, we investigated whether the effects of leptin on MT development are systemic or local. Materials and Methods: MMTV-TGF-? transgenic female mice were fed ad libitum from week 10 up to week 74. Protein expression levels of leptin, ObR, and ObRb were measured in the mammary tissue samples of 74-week old MMTV-TGF-? mice with and without MT (MT-positive/MT-negative) by Western blot analysis. Serum leptin levels were measured by using the mouse adipokine LINCOplex kit 96-well plate assay. Results: Protein expression levels of ObRb were significantly lower in MT as compared to control tissue of mammary gland. In addition, protein expression levels of leptin were significantly higher in the MT tissue of MT-positive mice compared to control tissue of MT-negative mice. However, ObR protein expression levels in tissues of mice with and without MT were similar. Serum leptin levels at different ages were not significantly different between the two groups. Conclusion: Leptin and ObRb in the mammary tissue may play a critical role in the mammary cancer development, while contribution of short ObR isoform may be less important. Copyright © Experimental Oncology, 2022.