TY - JOUR T1 - G protein-coupled receptor kinase 2 (GRK2) as a potential modulator of the hallmarks of cancer JF - Molecular Pharmacology JO - Mol Pharmacol DO - 10.1124/mol.116.107185 SP - mol.116.107185 AU - Laura Nogues AU - Clara Reglero AU - Veronica Rivas AU - Maria Neves AU - Petronila Penela AU - Federico Mayor Y1 - 2016/01/01 UR - http://molpharm.aspetjournals.org/content/early/2016/11/28/mol.116.107185.abstract N2 - Malignant features such as sustained proliferation, refractoriness to growth suppressors, resistance to cell death or aberrant motility and metastasis can be triggered by a variety of mutations and signaling adaptations. Signaling nodes can act as cancer-associated factors by cooperating with oncogene-governed pathways or participating in compensatory transduction networks to strengthen tumor properties. G-protein-coupled receptor kinase 2 (GRK2) is arising as one of such nodes. Via its complex network of connections with other cellular proteins, GRK2 contributes to the modulation of basic cellular functions such as cell proliferation, survival or motility, and is involved in metabolic homeostasis, inflammation or angiogenic processes. Moreover, altered GRK2 levels are starting to be reported in different tumoral contexts and shown to promote breast tumorigenesis or to trigger the tumoral angiogenic switch. The ability to modulate several of the hallmarks of cancer puts forward GRK2 as an onco-modifier, able to modulate carcinogenesis in a cell-type specific way. ER -