Table 1.

CCN4 expression in various tumors

Cancer type	Increase/decrease in tumor activity	CCN4 splice variant	Mechanism/pathway (if known)	Reference
Breast		–	–	14 15 17
Prostate		–	Paracrine secretion factors	18 19
Ovarian		–	–	11 20
Oral		– – – SNP	VEGF-C; integrins ανβ3 and α5β1 Hypomethylation	22,23 24 25 26
Esophageal		–	–	27 28
Gastric		–	Cyclin D1; EMT proteins	29
Liver	–	Multiple	pAKT, p53, MMP-2	35 36 37 38,39
Cholangiocarcinoma		WISP-1v	P38, ERK MAPK	40
Pancreatic		–	–	41
Lung	a –	SNPs	–	6 42 43 44
Melanoma			Stromal secretion	45
Osteosarcoma		–	MMP-2, MMP-9, ανβ3 integrin; activates ERK-MAPK, NF-κB VEGF-A; RAK, JNK, HIF-1a	48 49
Chondrosarcoma	–	WISP-1v, WISP-1vx	MMP-2; FAK, ERK, NF-κB	50 51
Glioblastoma		–	–	52
Neurofibromatosis		–	–	2
Hematopoietic		–	pAKT, pERK, Bcl2	54 58–60

Notes: The findings derived from the references cited in this review article are summarized in tabular form. In column 2, the green arrows indicate an increase in tumor cell proliferation, migration, or other pro-oncogenic activity, while the red arrows indicate a decrease in these activities. “ ” indicates an increase in tumor cell proliferation, migration, or other pro-oncogenic activity, while “ ” indicates a decrease in these activities.

^aNo association with patient survival.

Abbreviations: EMT, epithelial–mesenchymal transition; SNPs, single-nucleotide polymorphisms; MAPK, mitogen-activated protein kinase; MMP-2, matrix metalloproteinase-2; NF-κB, nuclear factor κB; VEGF-C, vascular endothelial growth factor C.