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PMID:15684064
| Citation |
Schoonjans, K, Dubuquoy, L, Mebis, J, Fayard, E, Wendling, O, Haby, C, Geboes, K and Auwerx, J (2005) Liver receptor homolog 1 contributes to intestinal tumor formation through effects on cell cycle and inflammation. Proc. Natl. Acad. Sci. U.S.A. 102:2058-62 |
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| Abstract |
Liver receptor homolog 1 (LRH-1) is an orphan nuclear receptor that synergizes with beta-catenin/T cell factor 4 signaling to stimulate intestinal crypt cell renewal. We evaluated here the impact of haploinsufficiency of LRH-1 on intestinal tumorigenesis by using two independent mouse models of human colon tumorigenesis. Haploinsufficiency of LRH-1 blunts intestinal tumorigenesis in the ApcMin/+ mice, a genetic model of intestinal cancer. Likewise, Lrh-1+/- mice are protected against the formation of aberrant crypt foci in the colon of mice exposed to the carcinogen azoxymethane. LRH-1 gene expression is reduced in tumors that express elevated levels of the proinflammatory cytokine TNF-alpha. Reciprocally, decreased LRH-1 expression in Lrh-1+/- mice attenuates TNF-alpha expression. Compared with normal human colon, expression and subcellular localization of LRH-1 is significantly altered in neoplastic colon. In combination, these data suggest a role of LRH-1 in the initiation of intestinal tumorigenesis both by affecting cell cycle control as well as through its impact on inflammatory pathways. |
| Links |
PubMed PMC548586 Online version:10.1073/pnas.0409756102 |
| Keywords |
Animals; Azoxymethane/pharmacology; Carcinogens/pharmacology; Cell Cycle/physiology; Disease Models, Animal; Female; Heterozygote; Humans; Inflammation/metabolism; Intestinal Neoplasms/chemically induced; Intestinal Neoplasms/metabolism; Intestinal Neoplasms/pathology; Male; Mice; Mice, Inbred C57BL; Receptors, Cytoplasmic and Nuclear/genetics; Receptors, Cytoplasmic and Nuclear/metabolism; Tumor Necrosis Factor-alpha/metabolism |
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Significance
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