Loss of TP53 cooperates with c-MET overexpression to drive hepatocarcinogenesis
We found that concomitant deletion of Trp53 and overexpression of c-MET (c-MET/sgp53) in the mouse liver led to HCC formation in vivo.  Subsequently, a stably passaged cell line derived from a c-MET/sgp53 HCC were generated. We then performed gene expression profiling analysis using data obtained from RNA-seq of the c-MET/sgp53 HCC cell line. Wild-type FVB/N mouse liver were used as control. Overall design: Comparative gene expression profiling analysis of RNA-seq data for the mouse HCC cell line (derived from c-MET/sgp53 mouse HCC) and wild-type FVB/N mouse liver.