The Nephroblastoma Overexpressed Gene (NOV/ccn3) Protein Associates with Notch1 Extracellular Domain and Inhibits Myoblast Differentiation via Notch Signaling Pathway

Activation of Notch1 signaling in stromal fibroblasts inhibits melanoma growth by upregulating WISP-1

“…WISP-1, also known as CCN4, was initially identified as a Wnt1-responsive target (Pennica et al, 1998), and belongs to the CCN family, which includes the connective tissue growth factor, cysteine-rich-61 (CYR61) and nephroblastoma overexpressed (NOV) (Sakamoto et al, 2002). Potential involvements of WISP-1 in several cancers have been reported (Soon et al, 2003;Chen et al, 2007;Davies et al, 2007), whereas its role in melanoma remains unexplored.…”

CCN1 (CYR61) and CCN3 (NOV) signaling drives human trophoblast cells into senescence and stimulates migration properties

“…This finding strongly corroborates our findings that CCN1 and CCN3 activate Notch-1 signaling and thereby reduce proliferation of the cytotrophoblast cell line SGHPL-5, as reported by Haider et al 41 CCN proteins are known to act via Notch-1 in other systems, such as myoblasts. [42][43][44][45] Our recent studies showed that Notch/p21 signaling also seems to mediate the proliferation-reducing activity of CCN3 in malignant Jeg3 cells. 14 In the present study we found that CCN1 and CCN3 cause a G0/G1 cell cycle arrest and induce cellular senescence in SGHPL-5 trophoblast cells; this effect is presumably mediated by activation of the Notch-1 receptor after upregulation of p21.…”

Periostin is required for matricellular localization of CCN3 in periodontal ligament of mice

“…The other constructs used were described previously (Sakamoto et al 2002;Tanabe et al 2010;Kii et al 2010). The protein tags, FLAG, HA, and human Fc (hFc), were placed in-frame at the C-terminus.…”