In conclusion our findings suggested that EP
In conclusion, our findings suggested that EP4 receptor activation triggers apoptosis in B-cell lymphoblasts. Our results also showed that EP4 receptor engagement inactivates NF-κB, which, in turn, sensitizes Ramos Chromocarb weight to apoptosis induced by chemotherapeutic agents. EP4 receptor agonists are currently being tested in various pathological settings, such as ulcerative colitis, asthma, kidney related diseases, bone remodulation and rheumatoid arthritis. Our study identifies the as yet unrecognized potential of the EP4 receptor agonist Pg1-OH as a chemo-sensitizing agent in B-cell leukemia. The specific down-regulation of NF-κB-dependent pathways in B-cell malignancies by the EP4 receptor agonists opens new possibilities for treatment and the optimization of current therapy.
Acknowledgments We thank Benedict Dries-Jenkins for proofreading the manuscript. This work was supported by the Slovenian Research Agency Grants BI-FR/08-10-003 and 1000-07-310183.