Mercedes Nadal-Serrano1, Jorge Sastre-Serra, Adamo Valle, Pilar Roca, Jordi Oliver. 1. Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS-IdISPa), Universitat de les IllesBalears, E07122 Palma de Mallorca, Illes Balears, Spain.
Abstract
BACKGROUND/AIMS: Large-scale epidemiological studies support a correlation between obesity and breast cancer in postmenopausal women. Circulating leptin levels are increased in obese and it has been suggested to play a significant role in mammary tumor formation and progression. Moreover, regulation of oxidative stress is another important factor in both tumor development and responses to anticancer therapies. The aim of this study was to examine the relationship between oxidative stress and chronic leptin exposure. METHODS: We treated MCF-7 breast cancer cells with 100 ng/mL leptin for 10 days and analyzed cell growth, ROS production and oxidative damage, as well as, some of the main antioxidant systems. Furthermore, since the hyperleptinemia has been associated with a worse pathology prognosis, we decided to test the influence of leptin in response to cisplatin anticancer treatment. RESULTS: Leptin signalling increased cell proliferation but reduced ROS production, as well as, oxidative damage. We observed an upregulation of SIRT1 after leptin exposure, a key regulator of stress response and metabolism. Additionally, leptin counteracted cisplatin-induced cytotoxicity in tumor cells, showing a decrease in cell death. CONCLUSION: Chronic leptin could contribute to the effective regulation of endogenous and treatment-induced oxidative stress, and it contributes to explain in part its proliferative effects.
BACKGROUND/AIMS: Large-scale epidemiological studies support a correlation between obesity and breast cancer in postmenopausal women. Circulating leptin levels are increased in obese and it has been suggested to play a significant role in mammary tumor formation and progression. Moreover, regulation of oxidative stress is another important factor in both tumor development and responses to anticancer therapies. The aim of this study was to examine the relationship between oxidative stress and chronic leptin exposure. METHODS: We treated MCF-7 breast cancer cells with 100 ng/mL leptin for 10 days and analyzed cell growth, ROS production and oxidative damage, as well as, some of the main antioxidant systems. Furthermore, since the hyperleptinemia has been associated with a worse pathology prognosis, we decided to test the influence of leptin in response to cisplatin anticancer treatment. RESULTS:Leptin signalling increased cell proliferation but reduced ROS production, as well as, oxidative damage. We observed an upregulation of SIRT1 after leptin exposure, a key regulator of stress response and metabolism. Additionally, leptin counteracted cisplatin-induced cytotoxicity in tumor cells, showing a decrease in cell death. CONCLUSION: Chronic leptin could contribute to the effective regulation of endogenous and treatment-induced oxidative stress, and it contributes to explain in part its proliferative effects.
Authors: Kuo Chen; Jin Zhang; Narasimha M Beeraka; Chengyun Tang; Yulia V Babayeva; Mikhail Y Sinelnikov; Xinliang Zhang; Jiacheng Zhang; Junqi Liu; Igor V Reshetov; Olga A Sukocheva; Pengwei Lu; Ruitai Fan Journal: Front Oncol Date: 2022-06-22 Impact factor: 5.738
Authors: Monserrat Olea-Flores; Juan Carlos Juárez-Cruz; Miguel A Mendoza-Catalán; Teresita Padilla-Benavides; Napoleón Navarro-Tito Journal: Int J Mol Sci Date: 2018-11-06 Impact factor: 5.923