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. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2009 Jan;8(1):110–118. doi: 10.1158/1535-7163.MCT-08-0719

Figure 6. Schematic representations of signal pathways in response to rosiglitazone-inhibited NSCLC cell growth.

Figure 6

The PPARγ ligand, rosiglitazone, inhibits α4 nAChR expression through activation of ERK and p38 MAPK signaling followed by induction of p53 expression in a PPARγ-independent signaling. This, in turn, partially blocks α4 nAChR-mediated nicotine-induced NSCLC cell proliferation.