Fractalkine/CX3CR1 induces apoptosis resistance and proliferation through the activation of the AKT/NF ‐κB cascade in pancreatic cancer cells

In this study, we performed an analysis to determine the effects of fractalkine/CX3CR1 on modulating apoptosis and explored the related mechanisms. The expression of fractalkine/CX3CR1 was detected by immunohistochemistry and western blotting. The levels of AKT/p‐AKT, BCL‐xl, and BCL‐2 were detected by western blotting. Then, the effects of exogenous and endogenous fractalkine on the regulation of tumour apoptosis and proliferation were investigated. The mechanism of fractalkine/CX3CR1 on modulating apoptosis in cancer cells through the activation of AKT/NF‐κB/p65 signals was evaluated. The effect of fractalkine on regulating cell cycle distribution was also tested. Fractalkine, AKT/p‐AKT, and apoptotic regulatory proteins BCL‐xl and BCL‐2 were highly expressed in human pancreatic cancer tissues. In vitro, fractalkine/CX3CR1 promoted proliferation and mediated resistance to apoptosis in pancreatic cancer cells. The antiapoptotic effect of fractalkine was induced by the activation of AKT/NF‐κB/p65 signalling in pancreatic cancer cells. The NF‐κB/p65 contributes to promote the expressions of BCL‐xl and BCL‐2 and reduce caspase activity, thereby inhibiting apoptotic processes. Treatment with fractalkine resulted in the enrichment of pancreatic cancer cells in S phase with a concomitant decrease in the number of cells in G1 phase. The present study demonstrated the function of fractalkine in the activation of the AKT/NF‐κB/p65 signalling cascade and me...
Source: Cell Biochemistry and Function - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research