Figure 2.

Pathogenicity and factors associated with the disruption of the normal cellular activity. Hyper-methylation of the CDH1 gene and mutational alteration in TP53 protein causes the impaired synthesis of E-cadherin. The truncated APC causes accumulation of β-catenin, which activates the β-catenin-dependent genes and Wnt pathway, altering normal cellular functions. The Wnt pathway after its activation causes the accumulation of β-catenins in cytoplasm and its translocation into the nucleus where it transcriptionally activates the transcription factors belonging to the TCF family. The recurrent mutation in RhoA is able to alter the RhoA pathway, which has a deleterious effect on E-cadherin.