In Silico Interaction and Docking Studies Indicate a New Mechanism for PML Dysfunction in Gastric Cancer and Suggest Imatinib as a Drug to Restore Function


Gastric cancer as one of the most common cancers worldwide has various genetic and environmental riskfactors including Helicobacter pylori (H.pylori) infection. Recently, loss of a tumor suppressor gene namedpromyelocytic leukemia (PML) has been identified in gastric cancer. However, no mutation has been found in thisgene in gastric cancer samples. Cag A H.pylori protein has been shown to exert post transcriptional regulationof some tumor suppressor genes. In order to assess such a mechanism for PML degradation, we performed insilico analyses to establish any interaction between PML and Cag A proteins. In silico interaction and dockingstudies showed that these two proteins may have stable interactions. In addition, we showed that imatinib kinaseinhibitor can restore PML function by inhibition of casein kinase 2.