c-Met activation leads to the establishment of a TGFb regulatory network required for bladder cancer invasion

Aberrant c-Met activation and upregulation of its cognate ligand HGF are frequently observed in bladder cancer and have been shown to regulate downstream pathways involved in proliferation, motility, and invasion. The precise mechanism underlying HGF/c-MET mediated invasion in bladder cancer is partly addressed by this microarray dataset. HGF activates the canonical TGFb signaling pathway to enhance epithelial mesenchymal transition and bladder carcinoma invasion.膀胱癌中常可观察到异常激活的c-Met及其同源配体肝细胞生长因子（hepatocyte growth factor, HGF）的表达上调，且已有研究证实二者可调控参与细胞增殖、迁移与侵袭的下游信号通路。本基因芯片数据集（microarray dataset）部分阐明了膀胱癌中HGF/c-MET介导肿瘤侵袭的具体分子机制。HGF可激活经典的转化生长因子β（transforming growth factor β, TGF-β）信号通路，进而增强上皮间质转化（epithelial-mesenchymal transition, EMT）并提升膀胱癌细胞的侵袭能力。