Anderson, PhilipErickson, LesWilliams, EugeneThomas, Logan2024-09-052024-09-052024http://hdl.handle.net/11603/36066Bladder cancer has a high prevalence throughout the world, primarily affecting men over the age of 55. Despite having multiple treatment options, such as chemotherapy, radiation, and surgery, bladder cancer has a high recurrence rate in patients. Consistent with other cancer types, understanding the molecular mechanism of bladder cancer has the potential to increase the number and type of treatment options available to patients. Upregulation of the transcription factor (TF), PPARγ, has been associated with the metastasis of bladder cancer, but this mechanism is not clearly understood. To gain additional information on this mechanism, we conducted both a ChIP-Seq and RNA-Seq analysis on three bladder cancer cell lines (UMUC1, SW780, and 5637) after treatment with a PPARγ agonist, rosiglitazone (RZ). The goal of this analysis is to identify genome-wide binding sites and genes regulated by PPARγ within these cell lines. We determined that RZ reduced the number of PPARγ binding sites in the three bladder cancer cell lines. Additionally, there were no PPARγ motifs bound by PPARγ regardless of cell or treatment type. The RNA-Seq results suggest that RZ affects gene expression within UMUC1 and SW780 cell lines but not 5637. Furthermore, GSEA identified numerous differentially expressed biochemical pathways in the UMUC1 and SW780 cell lines. G2M checkpoint and E2F target gene sets were downregulated within RZ-treated UMUC1 and SW780 cells but not 5637. The downregulation of these mechanisms may play an essential role in PPARγ’s involvement in bladder cancer metastasis. How PPARγ is involved in bladder cancer metastasis is still unknown; however, these results provide additional insight into this mechanism.95 pagesen-USBladder--CancerPPARγCancer metastasisCancer cell gene regulationText