Concurrent activation of RAS/ERK and PI3K/AKT pathways is implicated in prostate cancer progression. The negative regulators of these pathways, including sprouty2 (SPRY2), protein phosphatase 2A (PP2A), and phosphatase and tensin homolog (PTEN), are commonly inactivated in prostate cancer. The molecular basis of cooperation between these genetic alterations is unknown. Here, we show that
Rachana Patel, Meiling Gao, Imran Ahmad, Janis Fleming, Lukram B. Singh, Taranjit Singh Rai, Arthur B. McKie, Morag Seywright, Robert J. Barnetson, Joanne Edwards, Owen J. Sansom, Hing Y. Leung
SPRY2 deficiency induces TP53-dependent G1 arrest via nuclear PTEN.
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