We addressed whether: (a) the native tube forming capacity of the LEC on Matrigel is dependent on COX-2 or EP4 activity; (b) soluble products of COX-2-expressing breast cancer cells stimulate tube formation by the LEC; (c) proliferation, migration and tube forming capacity of the LEC are stimulated by exogenous PGE2 or selective EP4 agonists and if so, what are the underlying signaling mechanisms. The gene discussed is PTGS2; the disease is breast carcinoma.