Overexpression of WISP-1 Down-regulated Motility and Invasion of Lung Cancer Cells through Inhibition of Rac Activation

Soon, Lilian; Yie, Ting-An; Shvarts, Anita; Levine, Arnold J.; Su, Fei; Tchou-Wong, Kam-Meng

doi:10.1074/jbc.m210945200

Cited by 88 publications

(93 citation statements)

References 35 publications

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“…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. We sought to investigate the biological function of WISP-1 in melanoma.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2011

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Section: Discussionmentioning

confidence: 99%

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

et al. 2011

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“…These results suggest that EMMPRIN-mediated regulation of b-catenin signaling is independent of MMP regulation and perhaps MMP expression is downstream of the Wnt/b-catenin signaling pathway. However, we cannot exclude the possibility that b-catenin signaling and MMP induction are stimulated independently through two distinct and separate pathways, although there is evidence that MMP expression can be stimulated by Wnt signaling (Roth et al, 2000;Soon et al, 2003;Lowy et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

et al. 2010

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Advances in the field of tumor biology have identified that tumor cells co-opt developmental signaling pathways of embryonic stem cells and thus gain the ability to proliferate, differentiate and alter cell-cell interactions. One such pathway is the Wnt/b-catenin signaling pathway. High levels of EMMPRIN expression have been shown to correlate with poor prognosis and metastasis in a broad range of tumors. Although a variety of functions are attributed to EMMPRIN in tumorigenesis, the specific mechanism(s) through which it can exert its effects have not been elucidated, until now. In this study, we identify EMMPRIN as a novel regulator of the canonical Wnt/ b-catenin signaling pathway in lung cancer. Increasing EMMPRIN expression levels in lung cancer epithelial cells upregulated the b-catenin signaling pathway and silencing EMMPRIN inhibited b-catenin signaling, cell migration, proliferation, anchorage-independent growth and tumor growth in a mouse tumor xenograft model. These results provide a compelling rationale for targeting EMMPRIN for anticancer therapies. Understanding the molecular mechanisms driving EMMPRIN-induced lung tumorigenesis will provide enormous benefits in developing new therapeutic treatments for this and other forms of cancer.

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“…These interactions are mediated directly by specific adhesion receptors and indirectly by extracellular proteases, such as MMPs, proteolytic enzymes that regulate various cell behaviours, including cell growth, differentiation, apoptosis, migration and invasion. CCN proteins were reported to modulate the expression of MMP-1, -2, or -3 in relation to their pro-or anti-motility effects on different cell types (Fan and Karnovsky, 2002;Lake and Castellot, 2003;Laurent et al, 2003;Soon et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

et al. 2005

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Altered expression of CCN3 has been observed in a variety of musculoskeletal tumours, including Ewing's sarcoma (ES). Despite its widespread distribution, very little is known about its biological functions and molecular mechanisms of action. We transfected CCN3 gene into a CCN3-negative ES cell line and analysed the in vitro and in vivo behaviours of stably transfected clones. Forced expression of CCN3 significantly reduced cell proliferation in vitro, growth in anchorage-independent conditions, and tumorigenicity in nude mice. Despite the antiproliferative effect, CCN3-transfected ES cells displayed increased migration and invasion of Matrigel. The decreased expression of a2b1 integrin receptor and the increased amount of cell surface-associated matrix metalloproteinase (MMP)-9 following the expression of CCN3 may be the basis for the increased migratory abilities of transfected cells. Cells lacking a 2 b 1 are less facilitated to have stable anchorage since the predominant collagen extracted from ES tissue is indeed type I collagen, and proMMP-9 was recently found to provide a cellular switch between stationary and migratory ES cell phase. Our findings are in line with those recently obtained in glioblastoma. However, the underlying molecular mechanisms appear to be different, further highlighting the importance of the cellular context in the regulation of function of CCN proteins.

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Overexpression of WISP-1 Down-regulated Motility and Invasion of Lung Cancer Cells through Inhibition of Rac Activation

Cited by 88 publications

References 35 publications

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

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

EMMPRIN regulates the canonical Wnt/β-catenin signaling pathway, a potential role in accelerating lung tumorigenesis

In Ewing's sarcoma CCN3(NOV) inhibits proliferation while promoting migration and invasion of the same cell type

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