Apart from the steady-state increase of PGE2, the absence of sPLA2-III markedly attenuates the tumor-associated induction of PGE2-biosynthetic enzymes (COX-2 and mPGES-1), implying the reduced biosynthesis of pro-tumorigenic PGE2 in the colon cancer state. Here, PTGS2 is linked to colonic neoplasm.