G B Gelaleti1,2, T F Borin3, L B Maschio-Signorini2, M G Moschetta2, E Hellmén4, A M Viloria-Petit5, D A P C Zuccari1,2. 1. Programa de Pós-Graduação em Genética, Universidade Estadual Paulista 'Júlio de Mesquita Filho' (UNESP/IBILCE), São José do Rio Preto, Brazil. 2. Faculdade de Medicina de São José do Rio Preto (FAMERP), Laboratório de Investigação Molecular do Câncer (LIMC), São José do Rio Preto, Brazil. 3. Georgia Cancer Center, Tumor Imaging Angiogenesis Laboratory, Augusta University, Augusta, Georgia. 4. Department of Anatomy, Physiology and Biochemistry, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden. 5. Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Canada.
Abstract
BACKGROUND: Melatonin has oncostatic actions and IL-25 is active in inflammatory processes that induce apoptosis in tumor cells AIM: The aim of this study was to evaluate melatonin and IL-25 in metastatic (CF-41) and non-metastatic (CMT-U229) canine mammary tumor cells cultured as monolayers and tridimensional structures. MATERIALS AND METHODS: The cells were treated with melatonin, IL-25 and IL-17B silencing gene and performed cell viability, gene and protein expression of caspase-3 and VEGFA (Vascular endothelial growth factor A) and an apoptosis membrane protein array. RESULTS: Treatment with 1 mM of melatonin reduced cell viability of both tumor cell lines, all treatments alone and combined significantly increased caspase-3 cleaved and proteins involved in the apoptotic pathway and reduced pro-angiogenic VEGFA, confirming the effectiveness of these potential promising treatments. CONCLUSION: This is the first study evaluating the potential use of these strategies in CF-41 and CMT-U229 cell lines and together encourages subsequent in vitro and in vivo studies for further exploration of clinical applications.
BACKGROUND:Melatonin has oncostatic actions and IL-25 is active in inflammatory processes that induce apoptosis in tumor cells AIM: The aim of this study was to evaluate melatonin and IL-25 in metastatic (CF-41) and non-metastatic (CMT-U229) canine mammary tumor cells cultured as monolayers and tridimensional structures. MATERIALS AND METHODS: The cells were treated with melatonin, IL-25 and IL-17B silencing gene and performed cell viability, gene and protein expression of caspase-3 and VEGFA (Vascular endothelial growth factor A) and an apoptosis membrane protein array. RESULTS: Treatment with 1 mM of melatonin reduced cell viability of both tumor cell lines, all treatments alone and combined significantly increased caspase-3 cleaved and proteins involved in the apoptotic pathway and reduced pro-angiogenic VEGFA, confirming the effectiveness of these potential promising treatments. CONCLUSION: This is the first study evaluating the potential use of these strategies in CF-41 and CMT-U229 cell lines and together encourages subsequent in vitro and in vivo studies for further exploration of clinical applications.