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

ABSTRACT:

Background

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.

Methods

Herein, the functional impact of expressing variant forms of the oncogenic Met receptor (Tpr-Met) that selectively recruit the adaptor proteins Grb2 or Shc was investigated in a model derived from normal intestinal epithelial cells (IEC-6). An RNA interference (RNAi) approach was used to define the requirement of Grb2 or Shc in Tpr-Met-transformed IEC-6 cells. Since Grb2 and Shc couple RTKs to the activation of the Ras/MEK/Erk and PI3K/Akt pathways, Erk and Akt ph

SUBMITTER: Pomerleau V 

PROVIDER: S-EPMC4234027 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature