Role of PKCepsilon and PKCalpha in the oncogenic signaling transduced by RTKs.
The FGFRs are RTKs expressed by tissue-specific alternative splicing in epithelial IIIb or mesenchymal IIIc isoforms. In the epithelial-context, while FGFR2b acts as tumor suppressor, FGFR2c appears to play an oncogenic role. Based on our recent observation that the FGFR2b/FGFR2c switching and the ectopic expression of FGFR2c induce EMT and tumorigenic features in human keratinocytes, in this project we plan to investigate the possible involvement of PKCepsilon and PKCalpha downstream pathways in these FGFR2c-induced pathological outcomes. Our research project would significantly help to clarify the network of oncogenic pathways activated downstream FGFR2c in epithelial context, contributing to the advancement of knowledge of the complex molecular events underlying RTK signaling deregulation during carcinogenesis.