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Loss of the tumor suppressor PTEN is a common occurrence in prostate cancer. This aberration leads to the ectopic activation of the PI3K-Akt pathway, which promotes tumor growth. Here, we show that the transcription factor Gata3 is progressively lost in  Pten -deficient mouse prostate tumors as a result of both transcriptional down-regulation and increased proteasomal degradation. To determine the significance of this loss, we used conditional loss- and gain-of-function approaches to manipulate Gata3 expression levels in prostate tumors. Our results show that  Gata3  inactivation in  Pten -deficient prostates accelerates tumor invasion. Conversely, enforced expression of  GATA3  in  Pten -deficient tissues markedly delays tumor progression. In  Pten -deficient prostatic ducts, enforced GATA3 prevented Akt activation, which correlated with the down-regulation of  Pik3cg  and  Pik3c2a  mRNAs, encoding respectively class I and II PI3K subunits. Remarkably, the majority of human prostate tumors similarly show loss of active GATA3 as they progress to the aggressive castrate-resistant stage. In addition, GATA3 expression levels in hormone-sensitive tumors holds predictive value for tumor recurrence. Together, these data establish Gata3 as an important regulator of prostate cancer progression.

Gata3 antagonizes cancer progression in Pten -deficient prostates