MED10 and bladder transitional cell carcinoma: Furthermore, to confirm the functional and/or modulatory nature of the demonstrated MED10/hsa-miR-590-5p interaction, using agarose gel electrophoresis, we showed that the ectopic expression of MED10 in normal human primary bladder epithelial BdEC cells significantly upregulated the expression of hsa-miR-590, compared to the WT cells; more so, upon silencing MED10 (shMED10) in metastatic human bladder transition cell carcinoma SW1738 cells, hsa-miR-590 expression was markedly suppressed (Figure 4E).