Prostaglandin E2 receptor subtype 2 (EP2) null mice are protected against murine lung tumorigenesis.

Keith RL, Geraci MW, Nana-Sinkam SP, Breyer RM, Hudish TM, Meyer AM, Malkinson AM, Dwyer-Nield LD
Anticancer Res. 2006 26 (4B): 2857-61

PMID: 16886605

BACKGROUND - Manipulating prostaglandin (PG) production modulates tumor development. Elevated PGI2 production prevents murine lung cancer, while decreasing PGE2 content protects against colon cancer. PGE2 receptor subtype 2 (EP2) -deficient mice were hypothesized to be resistant to lung tumorigenesis.

MATERIALS AND METHODS - EP2 null BALB/c mice and their wild-type littermates were exposed to an initiation-promotion carcinogenesis protocol and lung tumorigenesis was examined. Chronic lung inflammation was induced to determine whether EP2 ablation influenced inflammatory cell infiltration.

RESULTS - Tumor multiplicity in EP2 null mice was 34% lower than in their wild-type littermates (21.9+/-3.0 vs. 14.5+/-2.9 tumors/mouse, p<0.001). The lung tumor burden, an indicator of growth rate, also declined (57%, p<0.05). All the mice exhibited similar inflammatory cell infiltration.

CONCLUSION - PGE2, acting through EP2, enhanced lung tumorigenesis through a mechanism that may be distinct from its proinflammatory activity. Thus, EP2 is a potential target for novel chemoprevention strategies.

MeSH Terms (13)

Animals Butylated Hydroxytoluene Cell Growth Processes Female Leukocytes Lung Neoplasms Male Methylcholanthrene Mice Mice, Inbred BALB C Mice, Knockout Receptors, Prostaglandin E Receptors, Prostaglandin E, EP2 Subtype

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