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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Cell Death Differ. 2009 Oct 16;17(3):469–481. doi: 10.1038/cdd.2009.148

Figure 7. Disruption of PPARγ resulted in mouse prostate carcinogenesis involving oxidative stress and autophagy.

Figure 7

The simplified diagram brings together data from the studies and presents a model illustrating how the PPARγ signaling contributes to prostate carcinogenesis from wild-type to mPIN formation and to set up conditions that would predispose cells to further malignant progression. These data suggested an important role for the PPARγ gene in maintaining the maturation, differentiation and turnover of subcellular organelles (peroxisomes, mitochondria and lysosomes) during mouse prostatic organogenesis and development. In particular this model suggests that a mechanism by which loss of PPARγ could lead to mouse PIN related to the disruption of cellular peroxisomal and mitochondrial lipid metabolism and oxidative stress (hypoxia) and active autophagy for the extended life span and cellular dedifferentiation.