The number of colonic ACF or intestinal polyps in mouse models of intestinal tumorigenesis following either genetic deletion or pharmacologic inhibition of EP receptor subtypes or COX isoforms
Receptor | Azoxymethane-Induced ACF Development* | ApcMin/+ Mouse Polyposis† | ApcΔ716 Mouse Polyposis† |
---|---|---|---|
EP1 | 65% (GD; ref. 70) | 56% (P; ref. 70) | No difference (GD; ref. 68) |
65% (P; refs. 70, 71) | No Δ polyp size | ||
EP2 | ND | ND | 58% (GD; ref. 68) |
EP3 | No difference (GD; ref. 67) | ND | No difference (GD; ref. 68) |
EP4 | 56% (GD; ref. 67) | 69% (P; ref. 67) | No difference (EP4+/− only; ref. 68) |
67% (P; ref. 67) | Polyp size decreased | ||
COX-1 | 60% (P; ref. 72) | 23% (GD; ref. 5) | 59%‡ (P; ref. 72) |
COX-2 | 63% (P; ref. 73) | 16% (GD; ref. 5) | 14% (GD; ref. 76) |
3%§ (P; ref. 74) | 29% (P; ref. 75) | 45% (P; refs. 77, 78) | |
Anti-PGE2 antibody | ND | 67% (63) | ND |
No Δ polyp size |
NOTE: ND, not determined.
↵* Azoxymethane-induced ACF number following either genetic deletion (GD) or pharmacologic inhibition (P) as a percentage of wild-type or control ACF multiplicity.
↵† Polyp (or adenoma) number following either genetic deletion (GD) or pharmacologic inhibition (P) as a percentage of wild-type or control polyp multiplicity. Δ, change.
↵‡ The Apc1309 mouse model of familial adenomatous polyposis was used in this study.
↵§ Percentage of azoxymethane-induced tumor (not ACF) multiplicity in untreated rats.