The aim of this master’s thesis was to investigate the effects of the retinoids all-trans retinoic acid (ATRA) and fenretinide on the viability, migration, and proliferation of normal urothelial SV-HUC1 cells and T24 urothelial cancer cells in vitro. Cell viability was assessed using an ATP assay, migration using a wound-healing assay, proliferation by immunofluorescence staining of Ki-67, and the expression of selected genes by quantitative real-time polymerase chain reaction. Both retinoids reduced the viability of both cell lines, with a more pronounced effect observed after longer treatment. Fenretinide reduced the viability of T24 cancer cells more strongly than that of normal SV-HUC1 cells, whereas the difference between the two cell lines was less pronounced following ATRA treatment. The most pronounced difference between cancer and normal cells was observed at 5 µM fenretinide, which reduced the viability of T24 cells while largely preserving the viability of SV-HUC1 cells. Both retinoids inhibited cell migration in both cell lines; however, the response of normal SV-HUC1 cells was more consistent, whereas the response of T24 cells depended on the type and concentration of the retinoid and the duration of treatment. The two retinoids also differed in their effects on proliferation; ATRA reduced the proportion of proliferating T24 cells, whereas fenretinide increased it. After 6 hours of treatment, no statistically significant changes in the expression of the analysed genes were detected. These results indicate that the effects of retinoids on urothelial cells depend on the type of retinoid, its concentration, exposure time, and the characteristics of the cell line.
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