The diagnosis and management of bladder cancer (BC) are high complex due to cancer heterogeneity among patients. Thus, biomarkers play pivotal roles in the diagnosis, prognosis determination, and planning of therapeutic intervention of BC. With years of research and discovery, many candidate markers for BC have emerged. The alterations of nucleosides, proteins, post-translational modifications, and cells are the candidate markers for early diagnosis and post-operative recurrence monitoring of BC. This review mainly discusses the recent progresses in the proteins and nucleosides markers for diagnosis and recurrence monitoring of BC. In the detection of BC, some potential nucleoside-based markers have been reported, including telomerase reverse transcriptase (TERT) gene, microsatellite, and chromosome instability, whereas the protein markers include bladder tumor antigen, nuclear matrix protein family (Nuclear matrix protein 22), fibrin/fibrin degradation product, and aberrantly glycosylated integrin α3β1. Besides, the performance of diagnostic methods based on these markers are reviewed. The sensitivity and specificity of candidate markers and detection methods of BC are compared. In summary, this review provides invaluable information about the early diagnosis and recurrence of BC, which guides the development and improvement of novel markers for early diagnosis and post-operative recurrence monitoring of BC in future.
Glabridin (GLA) has a variety of biological activities and therapeutic effects in cancers. Whereas the effect of GLA on urothelial bladder carcinoma (UBC) cells and its underlying mechanisms remain unknown. The study revealed the effect of GLA on UBC and the potential mechanism of inducing cell apoptosis in vivo and in vitro. After treated with different concentrations of GLA, the cell activity decreased in a time‐ and dose‐dependent manner. The IC50 values of BIU‐87 and EJ cells at 48 h were 6.02 μg/ml (18.6 μm) and 4.36 μg/ml (13.4 μm), respectively. Additionally, GLA‐induced apoptosis and cycle arrest of BIU‐87 and EJ cells in G2 phase. Furthermore, wound healing experiments showed that GLA significantly reduced the migration activities of BIU‐87 and EJ cells. Mechanically, GLA obviously increased the expression of BIM, BAK1, and CYCS in both mRNA and protein levels, which led to the activation of the endogenous apoptotic pathway. Finally, GLA remarkably inhibited the growth of UBC tumors in vivo. In summary, GLA inhibited UBC cells growth in vitro and in vivo by inducing cell apoptosis and cell cycle arrest, highlighting that GLA could be utilized as a component to design a novel anti‐UBC drug.
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