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e., Wdr77 is translocated through the nucleus in to the cytoplasm to drive proliferation of prostate cancer cells. With this analyze, we used in vivo genetic studies to even further examine the position of Wdr77 in prostate tumorigenesis. We uncovered that prostate-unique deletion of Wdr77 abolished prostate tumor initiation induced by lack of the tumor suppressor Pten. Mechanistically, Wdr77 ablation inhibited E2F3 activation and Increased TGFβ signaling, resulting in attenuated cellular proliferation induced by loss of Pten. These findings set up a essential purpose of Wdr77 for prostate tumor initiation.
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