RT Journal Article
SR Electronic
T1 G-Protein–Coupled Receptor Kinase 2 as a Potential Modulator of the Hallmarks of Cancer
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 220
OP 228
DO 10.1124/mol.116.107185
VO 91
IS 3
A1 Laura Nogués
A1 Clara Reglero
A1 Verónica Rivas
A1 María Neves
A1 Petronila Penela
A1 Federico Mayor, Jr.
YR 2017
UL http://molpharm.aspetjournals.org/content/91/3/220.abstract
AB 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 oncomodifier, able to modulate carcinogenesis in a cell-type specific way.