Table 1.

Roles of GRKs in different cancer types

Cancer	GRK isoform	Change	Functional effect	Reference
Glioblastoma multiforme	GRK3	Down	Increased growth of two different GBM cell lines	[37]
	GRK5	Up	Positively correlated with aggressiveness of glioma. Increased the proliferation rate of GSC	[38]
Medulloblastoma	GRK6	Down	Enhanced cell migration and CXCL12-mediated phosphorylation of ERK	[39]
Thyroid carcinoma	GRK2	Up	Reduction in proliferation of two poorly differentiated thyroid cell lines	[41]
	GRK5	Down	Defect in homologous desensitization of the TSH receptor	[40]
Breast cancer	GRK2	Up	Maintenance of tumoral proliferation and survival through regulating HDAC6/Pin1 axis	[42]
	GRK3	Down	Increase of CXCR4-mediated invasion and metastasis of breast cancer cell	[47]
	GRK4	Up	Enhanced cell proliferation by activation of ERK and JNK through β-arrestin	[48]
Ovarian neoplasm	GRK2, GRK4 γ/δ	Up	Elevated in granulosa cell tumors	[49]
Prostate cancer	GRK2	Down	Trigger androgen-independent tumor growth	[51]
	GRK3	Up	Increased angiogenesis, prostate tumor growth and metastasis	[52, 53]
	GRK5	Up	Increased proliferation, invasion, and metastasis of prostate cancer	[17, 54, 55]
Colorectal cancer	GRK5	Down	Increased proliferation regulated by TIG1	[57]
Hepatocellular carcinoma	GRK2	Down	Increased cell proliferation, migration and invasion	[58–61]
Pancreatic cancer	GRK2	Up	Accelerated cell growth. Predictive for poor overall survival of pancreatic cancer	[62, 63]
Lung cancer	GRK6	Down	Promoted tumor angiogenesis by upregulating MMP-2, MMP-9 release. Decreased survival	[64, 65]
Oral squamous cell carcinoma	GRK3	Up	Tumor malignancy and invasion	[67]
Multiple myeloma	GRK6	Up	Increased survival by enhanced phosphorylation of STAT3	[68]
Kaposi’s sarcoma	GRK2	Down	Enhanced migration and invasion of endothelial cells via activation of CXCR2/Akt	[69]
Osteosarcoma	GRK5	Up	Decreased apoptosis by phosphorylating p53 and promoting its degradation	[71]