Met receptor-induced Grb2 or Shc signals both promote transformation of intestinal epithelial cells, albeit they are required for distinct oncogenic functions

Deregulation of receptor tyrosine kinases (RTK) contributes to the initiation and progression of intestinal-derived epithelial cancers, including colorectal cancer (CRC). However, the roles of the proximal signaling molecules engaged by RTKs in different oncogenic functions of CRC remain unclear.