期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 14, 页码 -出版社
MDPI
DOI: 10.3390/ijms23147526
关键词
colorectal cancer; genistein; cell viability; hydrogen peroxide production; mitochondrial biogenesis; inflammation
资金
- Fondo de Investigaciones Sanitarias of Instituto de Salud Carlos III of the Spanish Government [PI14/01434]
- FEDER-Union Europea (Una manera de hacer Europa)
- Programa postdoctoral Margalida Comas-Comunidad Autonoma de las Islas Baleares [PD/050/2020]
Genistein may increase oxidative stress and inflammation in colon cancer cells, ultimately decreasing cell viability.
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 (H2O2) 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-kappa B translocation were determined by confocal microscopy. Genistein 100 mu M decreased cell viability and produced G(2)/M arrest, increased H2O2, and produced filopodia in SW620 cells. In HT29 cells, genistein produced an increase of cell death, H2O2 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-kappa B 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.
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