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PTEN  is frequently mutated in prostate cancer. The tumor suppressor function of PTEN is attributed to its lipid phosphatase activity that counters PI3K action. Here, we report a PTEN-ARID4B-PI3K axis in which PTEN inhibits expression of  ARID4B , while ARID4B is a transcriptional activator of the PI3K subunit genes  PIK3CA  and  PIK3R2  that are crucial for activation of the PI3K/AKT pathway. Reciprocal binding of ARID4B and histone H1 to the  PIK3CA  and  PIK3R2  promoters modulates chromatin condensation, suggesting a mechanism by which ARID4B activates these promoters. Functional analyses reveals that ARID4B is required for prostate tumorigenesis when PTEN is deficient. The biological significance is further substantiated by the existence of a  PTEN / ARID4B / PIK3CA  three-gene signature that improves the predictive power for prostate cancer recurrence in patients. In summary, we identify ARID4B as a master regulator in the PTEN-PI3K pathway, thus providing a potential therapeutic target for prostate cancer carrying  PTEN  mutations.

Identification of the PTEN-ARID4B-PI3K pathway reveals the dependency on ARID4B by PTEN-deficient prostate cancer