Comparison of mutational profiles for the major gastric cancer subtypes showed that RHOA mutations occur specifically in DGCs, the majority of which were histopathologically characterized by the presence of poorly differentiated adenocarcinomas together with more differentiated components in the gastric mucosa.
The top perturbed pathways in gastric cancer included adherens junction and focal adhesion, in which RHOA and other mutated genes we identified participate as key players.
In the present study, we have analyzed the expression status of the RhoA protein in human gastric cancer cells and tissues and investigated the possible involvement of RhoA in regulating the malignant phenotype of gastric cancer cells.