Activated PPAR𝛾 Targets Surface and Intracellular Signals That Inhibit the Proliferation of Lung Carcinoma Cells

Table 1

PPARγ-dependent signals in mediating the effects of PPARγ ligands.

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(1) PPARγ ligands inhibit cancer cell growth and induce apoptosis via:

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↓ PGE₂receptors (e.g., EP2 and EP4)

↑ Tumor suppressors (e.g., PTEN, p21)

↓ Inflammatory factors (e.g., NF-κB, MCP-1, COX-2)

↓ Angiogenic factors (e.g., VEGF)

↓ Survival factors (e.g., 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-9)

↓ Integrin receptors (e.g., α5β1)

↑↓ Others (e.g., cytokines (e.g., IL-13, IL-21, TGF-β1) and chemokines (e.g., MIP-1β))

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