| Autor: |
Alorda-Clara M; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain., Torrens-Mas M; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain.; Translational Research in Aging and Longevity (TRIAL) Group, Instituto de Investigación Sanitaria Illes Balears (IdISBa), E-07120 Palma de Mallorca, Illes Balears, Spain., Morla-Barcelo PM; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain., Roca P; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain.; Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto Salud Carlos III, E-28029 Madrid, Madrid, Spain., Sastre-Serra J; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain.; Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto Salud Carlos III, E-28029 Madrid, Madrid, Spain., Pons DG; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain., Oliver J; Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma de Mallorca, Illes Balears, Spain.; Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma de Mallorca, Illes Balears, Spain.; Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto Salud Carlos III, E-28029 Madrid, Madrid, Spain. |
| Abstrakt: |
Genistein could play a crucial role in modulating three closely linked physiological processes altered during cancer: oxidative stress, mitochondrial biogenesis, and inflammation. However, genistein's role in colorectal cancer remains unclear. We aimed to determine genistein's effects in two colon cancer cells: HT29 and SW620, primary and metastatic cancer cells, respectively. After genistein treatment for 48 h, cell viability and hydrogen peroxide (H 2 O 2 ) production were studied. The cell cycle was studied by flow cytometry, mRNA and protein levels were analyzed by RT-qPCR and Western blot, respectively, and finally, cytoskeleton remodeling and NF-κB translocation were determined by confocal microscopy. Genistein 100 µM decreased cell viability and produced G 2 /M arrest, increased H 2 O 2 , and produced filopodia in SW620 cells. In HT29 cells, genistein produced an increase of cell death, H 2 O 2 production, and in the number of stress fibers. In HT29 cells, mitochondrial biogenesis was increased, however, in SW620 cells, it was decreased. Finally, the expression of inflammation-related genes increased in both cell lines, being greater in SW620 cells, where NF-κB translocation to the nucleus was higher. These results indicate that high concentrations of genistein could increase oxidative stress and inflammation in colon cancer cells and, ultimately, decrease cell viability. |
