Copyright ©2010 Baishideng Publishing Group Co.
World J Biol Chem. Mar 26, 2010; 1(3): 31-40
Published online Mar 26, 2010. doi: 10.4331/wjbc.v1.i3.31
Table 1 PPARγ-dependent signals mediate the effects of PPARγ ligands in lung cancer cells
PPARγ ligands inhibit cancer cell growth and induce apoptosis via:
↓PGE2 receptors (e.g. EP2 and EP4)
↑Tumor suppressors (e.g. PTEN, p21, AP-2α, p53)
↓Inflammatory factors (e.g. NF-κB, MCP-1, COX-2)
↓Angiogenic factor (e.g. VEGF)
↓Survival factors (e.g. SAPK/JNK, ILK, Src, FAK, PI3-K/Akt, mTOR)
↑↓Other kinase signals (e.g. ERK, p38 MAPK)
↓Growth factor receptors (e.g. EGF-R, PDGF-R)
↓Extracellular matrices (e.g. Fibronectin, MMP-2, MMP-9)
↓Integrin receptors (e.g. α5β1)
↑↓Others [e.g. cytokines (e.g. IL-13, IL-21, TGF-β1) and chemokines (e.g. MIP-1β)]
↓Bcl-1, c-IAP2, etc.
PPARγ ligands stimulate cancer cell growth and reduce apoptosis via:
↑Wnt signaling and oncogenes (e.g. cyclin D1, β-catenin, c-Myc)
↑Angiogenic signaling (e.g. VEGF, Angptl4)