Studying potential PKCδ loss of function mutation and its downstream effects in gastric cancer progression

PKC isozymes are involved in the modulation of cellular pathways related with tumor progression, acting as a suppressor or promoter. In cancer cells, PKCs mutated, and most common type is loss function. This paper focuses on effect PKCδ mutation gastric cancer. LOF occurs throughout catalytic kinase domains PKCδ, disrupting activation function kinase. domain, there various potential targets, such binding groove zinc finger. Mutation residues detected DFG APE motifs, can alter function, causing interruption activation. Also, critical region, called hinge modulates caspase-3 dependent cleavage, tyrosine this region reduces cleavage activity, inhibiting fully Importantly, affects activity downstream protein, p53, through transcription, localization, phosphorylation. For instance, C1 domain mutant suppresses capacity reducing transcription p53. Disruption component, tight junction, assembling to mutation. As identified, correlates ZO-1, prevent translocation ZO-1 TJ area, leading errors assembling, promoting invasion.