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e., Wdr77 is translocated from the nucleus into the cytoplasm to travel proliferation of prostate cancer cells. In this review, we used in vivo genetic experiments to even further investigate the role of Wdr77 in prostate tumorigenesis. We located that prostate-specific deletion of Wdr77 abolished prostate tumor initiation induced by lack of the tumor suppressor Pten. Mechanistically, Wdr77 ablation inhibited E2F3 activation and Improved TGFβ signaling, resulting in attenuated mobile proliferation induced by loss of Pten. These results build a crucial job of Wdr77 for prostate tumor initiation.
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