To Live or to Die: Prosurvival Activity of PPAR𝜸 in Cancers

Figure 1

Schematic diagram showing how PPAR𝛾 increases cell survival in growth factor/nutrient-deprived cells. Growth factor/nutrient withdrawal induces ROS production. In the absence of PPAR𝛾 activation, increased levels of ROS inhibit mitochondrial electron transport, leading to mitochondrial depolarization, caspase activation, and cell death. When PPAR𝛾 is activated, the increase in ROS is attenuated by the receptor through transcriptional upregulation of cell type specific antioxidant factors, such as catalase, Cu/Zn-SOD (SOD1), Mn-SOD (SOD2), or UCP2. The transcriptional upregulation of these genes by PPAR𝛾 may or may not be direct (shown to be direct in the diagram for simplicity).