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Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors with essential functions in regulating lipid metabolism. Both the PPARs (also referred to as PPARδ) and PPARγ subtype have been reported to either attenuate or potentiate tumorigenesis in a number of different models of intestinal and skin carcino- genesis. In the present study, we have addressed the role of PPARs and PPARγ in lung tumorigenesis in a transgenic mouse model of RAF-induced lung adenoma using two different strategies: i) crossing with PPARs null mice, and ii) chronic treatment with the PPARγ agonist rosiglitazone. Histological examination revealed a significant enhancement of tumor growth in mice lacking one or both alleles of Pparb, but no significant effect in response to rosiglitazone. These observations indicate i) that RAF-induced lung tumorigenesis is attenuated in mice with a disrupted Pparb gene, and ii) that chronic PPARγ activation does not affect lung adenoma growth. These results are relevant with respect to the clinical application of drugs modulating the activity of PPARs or PPARγ.

Growth of transgenic RAF-induced lung adenomas is increased in mice with a disrupted PPARβ/δ gene