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PPARγ Agonist Suppresses TLR4 Expression and TNF-α Production in LPS Stimulated Monocyte Leukemia Cells

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Abstract

It has been well established that inflammation plays a critical role in cancer. Chronic inflammation promotes tumorgenesis and metastasis, which suggests that anti-inflammation drugs could act as a tumor suppressor. It is known that the peroxisome proliferator-activated receptor γ (PPARγ) has been implicated in anti-inflammatory responses; however, the anti-tumor effects of PPARγ have not been intensively investigated. In this study, we examined the effects of PPARγ in cancer. We show that the activation of PPARγ by its agonist rosiglitazone (RGZ) reduces cell proliferation rate in inflammatory and tumor-derived U937 cells. Treatment of RGZ suppresses the expression Toll-like receptor 4 (TLR4) and decreases the production of TNF-α in LPS treated U937 cells. This suggests that NF-κB signaling may be involved in anti-tumor effect of RGZ. Our results demonstrate a role of PPARγ in regulation of NF-κB signaling by modulating TLR4 expression and TNF-α production.

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Acknowledgments

We thank the members of our laboratories for their insight and technical support. This work was supported by the following fundings: National Natural Science Foundation of China (No.30770782), Natural Science Foundation of Guangdong Province (No.10151008901000243), Science and Technology Program of Guangzhou City (No. 2010J-E111) as well as Science and Technology Planning Project of Guangdong Province (No. 2010B030700006).

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Correspondence to Pei-Qing Liu or Jia-Jun Liu.

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Chun-Zhi Wang and Yong Zhang contributed equally to this study.

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Wang, CZ., Zhang, Y., Li, XD. et al. PPARγ Agonist Suppresses TLR4 Expression and TNF-α Production in LPS Stimulated Monocyte Leukemia Cells. Cell Biochem Biophys 60, 167–172 (2011). https://doi.org/10.1007/s12013-010-9136-6

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