Shp2 deletion in hepatocytes suppresses hepatocarcinogenesis driven by oncogenic β-Catenin, PIK3CA and MET.

ABSTRACT:

Background & aims

Shp2 is an SH2-tyrosine phosphatase acting downstream of receptor tyrosine kinases (RTKs). Most recent data demonstrated a liver tumor-suppressing role for Shp2, as ablating Shp2 in hepatocytes aggravated hepatocellular carcinoma (HCC) induced by chemical carcinogens or Pten loss. We further investigated the effect of Shp2 deficiency on liver tumorigenesis driven by classical oncoproteins c-Met (receptor for HGF), β-catenin and PIK3CA.

Methods

We performed hydrodynamic tail vein injection of two pairs of plasmids expressing c-Met and ΔN90-β-catenin (MET/CAT), or c-Met and PIK3CA^H1047R (MET/PIK), into WT and Shp2^hep-/- mice. We compared liver tumor loads and investigated the pathogenesis and molecular mechanisms involved using multidisc

SUBMITTER: Liu JJ 

PROVIDER: S-EPMC6008184 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature