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The PRL PTPs: Regulating Gene Expression to Reprogram the Cancer Cell

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Protein Tyrosine Phosphatases in Cancer

Abstract

Since the discovery of the PRLs in the 1990s, a large body of work has established that PRL overexpression endows cells with malignant properties and in human cancers is associated with disease progression and poor outcome. How the PRLs exert these effects at the molecular level remains unknown despite an intensive search for PRL substrates, including amongst components of key cancer-associated receptor-proximal signaling pathways. We discuss evidence to support a developing theme that the main action of the PRLs is to alter programs of gene expression. By so doing, the PRLs drive changes in molecular networks and cellular architecture to transform cell properties and advance cancer. We propose that defining and functionally investigating the PRL “interactome” could inform the mechanistic basis of PRL actions by revealing effectors and targeting partners to facilitate substrate identification. We also highlight recent findings on the actions of the PRLs gained from the first few studies in whole animal models, on regulation of the PRLs, and on progress towards therapeutic targeting of PRL-overexpressing tumors.

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Correspondence to Catherine J. Pallen .

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Rogers, C.A., Pallen, C.J. (2016). The PRL PTPs: Regulating Gene Expression to Reprogram the Cancer Cell. In: Neel, B., Tonks, N. (eds) Protein Tyrosine Phosphatases in Cancer. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-3649-6_10

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