Expression of prostaglandin G/H synthase-1 and -2 protein in human colon cancer.

TLDR

Prostaglandin G/H synthase (PGHS) produces prostaglandins and is targeted by NSAIDs; two isoforms, PGHS‑1 and PGHS‑2, have been identified, and epidemiologic data link NSAID use to reduced colorectal cancer risk. The study performed immunoblot analyses of PGHS‑1 and PGHS‑2 protein expression in 25 matched colon cancer and normal tissues, 4 premalignant polyps, 5 control colon samples, and 3 matched breast tissue pairs. PGHS‑1 was detected in all normal and tumor tissues, whereas PGHS‑2 was absent in 23 of 25 normal colon samples but present in 19 of 25 tumors and absent in premalignant polyps, control colon, and breast tissues, indicating NSAID protective effects may involve PGHS‑2 inhibition.

Abstract

Prostaglandin G/H synthase (PGHS), a key enzyme leading to the formation of prostaglandins, is the target of nonsteroidal antiinflammatory drugs. Two forms of the enzyme have been identified, PGHS-1 and PGHS-2. Epidemiological evidence has suggested that aspirin and other nonsteroidal antiinflammatory drugs may reduce the risk of colorectal cancer. We examined by immunoblot analyses the expression of human PGHS-1 and PGHS-2 protein in 25 matched colon cancer and nontumor tissues, 4 premalignant polyps, 5 control colon tissues from noncancer patients, and 3 matched normal and cancerous breast tissue samples. PGHS-1 was detected in all normal and tumor tissue. In contrast, PGHS-2 was not detected in 23 of 25 normal colon tissues but was detected in 19 of 25 colon tumors. PGHS-2 protein was not observed in four human premalignant polyp samples, control colon from noncancer patients, or matched normal or cancerous breast tissues. These results suggest that the beneficial effects of nonsteroidal antiinflammatory drugs in colon cancer may be mediated by inhibition of PGHS-2.