Helicobacter pylori CagA Suppresses Apoptosis through Activation of AKT in a Nontransformed Epithelial Cell Model of Glandular Acini Formation

Figure 4

AKT induced evasion of apoptosis correlates with BIM and BAD phosphorylation. (a) MCF-10A cell lysates were immunoblotted against AKT, BIM, and BAD and their phosphorylated forms (AKT in Ser473, BAD in Ser136, and BIM in Ser87). A densitometric analysis of phosphorylated proteins was normalized to the corresponding β-actin levels. An arbitrary value of 1 was assigned to the highest activity. (b) MCF-10A cells were infected with H. pylori strains in cell suspension and an AKT inhibitor was added; apoptosis was determined by anexin V and propidium iodide (PI) staining. (c) Percentage of living cells (Anexin V and PI negative). Representative assay of three independent experiments is shown. Asterisks denote statistical differences by the Student’s t-test, (^*p ≤ 0.05).

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