Anticancer actions of PPARγ ligands: Current state and future perspectives in human lung cancer

Table 2 PPARγ-independent signals triggered by PPARγ ligands in lung cancer cells

↑Tumor suppressors (e.g. LKB1, AMPK, TSC2)

↑ROS production and ERK, SAPK/JNK, p38 MAPK activation (note

that this also occurs in PPARγ-dependent pathways)

↓Effects on transcription factors (e.g. AP-1, NF-κB, Smads, Sp1, CRE)

↓Nicotine receptor signaling (e.g. α4 and α7 nAChRs)

↓Apoptosis-related signals (e.g. Bcl-2, cyclin D1, c-FLIP, DR-5)

↑Apoptosis-related signals (e.g. casease 3/7, cyclin D1, p53)

AMPK: AMP-activated protein kinase (AMPK); TSC2: Tuberous sclerosis complex 2.