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• W2314010547 abstract "RATIONALE: Pathways regulating lung cancer metastasis are not well understood. As with most cancers, metastasis depends on critical interactions between tumor cells and the surrounding tumor microenvironment. Peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor superfamily of ligand-activated transcription factors. In humans, a retrospective study of patients treated with thiazolidinediones (TZDs), which are ligands for PPARγ, demonstrated a 33% reduction in risk of developing lung cancer. However, the effect of PPARγ activation on progression and metastasis of established lung tumors has not been clearly established. Our laboratory has developed a mouse model in which murine lung cancer cells directly injected into the lung of syngeneic mice develop secondary pulmonary tumors and metastasize to the mediastinal lymph nodes, the liver, and the brain. The goal of this study was to assess the effects of the TZD pioglitazone on lung cancer progression using this model. METHODS: Murine non-small cell lung cancer cells stably transfected with firefly luciferase were implanted in the left lung of C57BL/6 wild-type mice. Mice were fed either chow impregnated with pioglitazone (0.05%) or control chow. At various time points following injection, animals were sacrificed and organs were assessed for tumors using ex vivo bioluminescence imaging. Primary tumors were measured with digital calipers, and the number of secondary tumors in the other lung lobes, liver and brain were quantified. RESULTS: There was no significant difference in the size of the primary tumor between pioglitazone-treated and control mice at one week. However, primary tumors were significantly larger in pioglitazone-treated animals both 16 and 22 days after implantation of cancer cells. The differences in pulmonary metastases were even more impressive. At both 7 and 16 days, pioglitazone-treated mice showed 2-3 times more secondary pulmonary tumors compared to control animals. By day 25-30, 37.5% of mice fed pioglitazone-impregnated chow developed liver metastases, whereas only 17.6% of mice fed normal chow developed liver metastases. Brain metastases were only detected in mice fed chow impregnated with pioglitazone. CONCLUSION: Treatment of mice with the PPARγ activator pioglitazone unexpectedly accelerates metastasis of established pulmonary tumors. Since selective activation of PPARγ in tumor cells has been shown to inhibit transformed growth and invasiveness, we hypothesize that the metastasis-promoting effects of pioglitazone are mediated through effects on the tumor microenvironment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2266." @default.
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• W2314010547 date "2010-04-15" @default.
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• W2314010547 title "Abstract 2266: Pioglitazone increases tumor progression and metastasis in an orthotopic mouse model of non-small cell lung cancer" @default.
• W2314010547 doi "https://doi.org/10.1158/1538-7445.am10-2266" @default.
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