Radiation resistance, invasiveness and metastasis are inflammatory events that could be suppressed by lipoxin A4

Radiation induces overexpression and activity of the MET oncogene that, in turn, enhances the production of prostaglandin E2, a pro-inflammatory molecule. Prostaglandin E2 promotes tumor cell invasion, prevents apoptosis, enhances their metastasis and causes radioresistance. It is proposed that lipoxin A4, a potent endogenous anti-inflammatory molecule, opposes the actions of prostaglandin E2 and thus, could promote radiosensitivity, suppress tumor cell proliferation, invasiveness and suppress metastasis. Thus, methods designed to enhance endogenous lipoxin A4 formation or its synthetic analogs may be useful in the management of cancer.