Figure 6 | Signal Transduction and Targeted Therapy

Figure 6

From: Analyses of publicly available genomics resources define FGF-2-expressing bladder carcinomas as EMT-prone, proliferative tumors with low mutation rates and high expression of CTLA-4, PD-1 and PD-L1

Figure 6

FGF-2 promotes the malignant progression of invasive bladder carcinomas by coupling two epigenetically controlled pathways: a model. FGF-2 induces the expression of KDM2B and EZH2. The Akt3 kinase, whose expression correlates with the expression of FGF-2 and may be regulated by this growth factor, promotes a shift in FGFR-2 alternative splicing toward the FGFR-2 IIIc splice form, which is recognized by FGF-2, thus enhancing the FGF-2 response. Finally, FGF-2 promotes EMT, cancer stem cell self-renewal and cell cycle progression. The mechanisms of KDM2B/EZH2 regulation by FGF-2 and the mechanism by which Akt3 regulates the alternative splicing of FGFR-2 have been published.6,11 The regulation of cell migration and invasiveness and the regulation of cancer stem cell self-renewal by KDM2B have also been described previously.11,12 Finally, the regulation of the cell cycle by KDM2B has been observed earlier, and it is supported by gene expression data in prior literature.33,55 EMT, epithelial to mesenchymal transition; FGF-2, fibroblast growth factor 2.

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