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 E(2), a pro-inflammatory molecule. Prostaglandin E(2) promotes tumor cell invasion, prevents apoptosis, enhances their metastasis and causes radioresistance. It is proposed that lipoxin A(4), a potent endogenous anti-inflammatory molecule, opposes the actions of prostaglandin E(2) and thus, could promote radiosensitivity, suppress tumor cell proliferation, invasiveness and suppress metastasis. Thus, methods designed to enhance endogenous lipoxin A(4) formation or its synthetic analogs may be useful in the management of cancer.