PP2A inhibitors induce apoptosis in pancreatic cancer cell line PANC-1 through persistent phosporylation of IKK and sustained activation of the NF-kB

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and OA is considered to be carcinogenic.

PP2A inhibitors, cantharidin and OA, had strong anti-tumor activities against pancreatic cancer cell line PANC-1 through persistent activation of the NF-kB pathway. Treatment with PP2A inhibitors induced phosphorylation of IKKa, phosphorylation and degration of IkBa, and nuclear translocation of p65. Activated NF-kB triggered apoptosis through extrinsic pathway and inhibited cellular viability. Cytotoxicity effect was probably due to the elevated expression of downstream pro-apoptotic genes.

In the present study, PP2A inihibitors induce extrinsic apoptosis and inhibit cell viability in pancreatic cancer cell line PANC-1 through persistent activation of the NF-kBpathway. The cytotoxity effect is probably due to the selective elevation of downstream pro-apoptotic genes. Our findings provide convincing evidence for how PP2A inihibitors carry out anti-tumor effects and reveal the possibility of using PP2A as a therapeutic target for ...

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