CASP3 and gastric adenocarcinoma: Finally, we looked for a molecular mechanism accounting for the reduced cell viability observed in the 23132/87 cells after the simultaneous silencing of poly-Ub genes UBC and UBB. Considering the role of the extrinsic pathway of apoptosis in gastric adenocarcinoma [39], we evaluated if the significant decrease (p = 0.004) in 23132/87 cell viability after treatment with the combination siUBB+siUBC could be linked to an increase in Fas levels [31] and activation of caspase 3.