G protein-coupled receptor kinases (GRKs) constitute seven subtypes of serine/threonine protein kinases that specifically recognize and phosphorylate agonist-activated G protein-coupled receptors (GPCRs), thereby terminating the GPCRs-mediated signal transduction pathway. Recent research shows that GRKs also interact with non-GPCRs and participate in signal transduction in non-phosphorylated manner. Besides, GRKs activity can be regulated by multiple factors. Changes in GRKs expression have featured prominently in various tumor pathologies, and they are associated with angiogenesis, proliferation, migration, and invasion of malignant tumors. As a result, GRKs have been intensively studied as potential therapeutic targets. Herein, we review evolving understanding of the function of GRKs, the regulation of GRKs activity and the role of GRKs in human malignant tumor pathophysiology.

中文翻译：

---

G蛋白偶联受体激酶在恶性肿瘤病理学中的作用。

G蛋白偶联受体激酶（GRK）构成丝氨酸/苏氨酸蛋白激酶的七个亚型，它们特异性识别并磷酸化激动剂激活的G蛋白偶联受体（GPCR），从而终止GPCR介导的信号转导途径。最近的研究表明，GRKs还与非GPCR相互作用，并以非磷酸化的方式参与信号转导。此外，GRK的活性可以受多种因素调节。GRKs表达的变化在各种肿瘤病理学中都具有突出的特征，并且它们与恶性肿瘤的血管生成，增殖，迁移和侵袭有关。结果，已经广泛研究了GRKs作为潜在的治疗靶标。在这里，我们回顾了对GRK功能的不断发展的理解，