The Nuclear Phosphoinositide-p53 Signalosome in the Regulation of Cell Motility
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Xiaoting Hou,
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Yu Chen,
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Bo Zhou,
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Fengting Liu,
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Lingyun Dai,
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Chunbo Chen,
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Noah D. Carrillo,
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Vincent L. Cryns,
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Richard A. Anderson,
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Jichao Sun,
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Mo Chen
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Abstract
Dysregulation of p53 and phosphoinositide (PIP<sub>n</sub>) signaling are both key drivers of oncogenesis and metastasis. Our recent findings reveal a previously unrecognized interaction between these pathways, converging in the nucleus to form a PIP<sub>n</sub>-p53 signalosome that modulates nuclear AKT activation and downstream signaling, thereby influencing cancer cell survival and motility. This review examines recent insights into nuclear PIP<sub>n</sub> signaling in the context of established roles for p53 in cell dynamics and migration while also deliberating current research on how nuclear PIP<sub>n</sub>s interact with p53 to form signalosomes that affect cell motility. We emphasize the critical role of PIP<sub>n</sub>s in stabilizing p53 and activating de novo nuclear AKT signaling, which subsequently modulates key motility-related pathways. Understanding the unique operation and function of the PIP<sub>n</sub>-p53 signalosome in nuclear phosphatidylinositol 3-kinase (PI3K)-AKT activation offers novel therapeutic strategies for controlling cancer metastasis by targeting pertinent interactions and events.
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