作者: Laura Nogués , Clara Reglero , Verónica Rivas , María Neves , Petronila Penela
关键词: Kinase 、 Angiogenic Switch 、 Cell biology 、 Cell growth 、 Biology 、 Receptor 、 Carcinogenesis 、 Beta adrenergic receptor kinase 、 The Hallmarks of Cancer 、 G protein-coupled receptor kinase
摘要: Malignant features—such as sustained proliferation, refractoriness to growth suppressors, resistance cell death or aberrant motility, and metastasis—can be triggered by a variety of mutations signaling adaptations. Signaling nodes can act cancer-associated factors cooperating with oncogene-governed pathways participating in compensatory transduction networks strengthen tumor properties. G-protein–coupled receptor kinase 2 (GRK2) is arising one such nodes. Via its complex network connections other cellular proteins, GRK2 contributes the modulation basic functions—such survival, motility—and involved metabolic homeostasis, inflammation, angiogenic processes. Moreover, altered levels are starting reported different tumoral contexts shown promote breast tumorigenesis trigger switch. The ability modulate several hallmarks cancer puts forward an oncomodifier, able carcinogenesis cell-type specific way.