Stromal Matrix Metalloproteinase-9 Regulates the Vascular Architecture in Neuroblastoma by Promoting Pericyte Recruitment

Chantrain, Christophe; Shimada, Hiroyuki; Jodele, Sonata; Groshen, Susan; Ye, Wei; Shalinsky, David R.; Werb, Zena; Coussens, Lisa M.; DeClerck, Yves A.

doi:10.1158/0008-5472.can-03-0160

Cited by 199 publications

(187 citation statements)

References 46 publications

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“…Our results are in accordance with those of previous reports showing that a high MMP-9 expression correlates significantly with tumoral aggressiveness and poor prognosis (Chantrain et al, 2004;Li et al, 2004;Pellikainen et al, 2004), as well as with other studies where high MMP-2 expression in carcinoma cells, in contrast, has been related to only a few inverse prognostic factors (Talvensaari-Mattila et al, 1998;Nakopoulou et al, 2003) or shown to have no association with clinicopathological parameters in breast cancer (Jones et al, 1999;Hirvonen et al, 2003;Talvensaari-Mattila et al, 2003). It has also been described that as breast cancer progresses, MMP-2 production increases during the early phases, whereas activation of MMP-9 occurs during the late cancerous stage (Liotta and Kohn, 2001), which could explain their different impact on prognosis in clinically detected invasive breast tumours.…”

Section: Discussionsupporting

confidence: 93%

Study of matrix metalloproteinases and their inhibitors in breast cancer

et al. 2007

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An immunohistochemical study was performed using tissue microarrays and specific antibodies against matrix metalloproteinases (MMPs) 1, 2, 7, 9, 11, 13, 14, and their tisullar inhibitors (TIMPs) 1, 2, and 3. More than 2600 determinations on cancer specimens from 131 patients with primary ductal invasive tumours of the breast (65 with and 66 without distant metastasis) and controls were performed. Staining results were categorised using a score based on the intensity of the staining and a specific software program calculated the percentage of immunostained cells automatically. We observed a broad variation of the total immunostaining scores and the cell type expressing each protein. There were multiple and significant associations between the expression of the different MMPs and TIMPs evaluated and some parameters indicative of tumour aggressiveness, such as large tumour size, advanced tumour grade, high Nottinham prognostic index, negative oestrogen receptor status, peritumoural inflammation, desmoplastic reaction, and infiltrating tumoural edge. Likewise, the detection of elevated immunohistochemical scores for MMP-9, 11, TIMP-1, and TIMP-2, was significantly associated with a higher rate of distant metastases. The expression of MMP-9 or TIMP-2 by tumour cells, MMP-1, 7, 9, 11, 13, or TIMP-3 by fibroblastic cells, and MMP-7, 9, 11, 13, 14, TIMP-1, or TIMP-2 by mononuclear inflammatory cells, was also significantly associated with a higher rate of distant metastases.

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Section: Discussionsupporting

confidence: 93%

Study of matrix metalloproteinases and their inhibitors in breast cancer

et al. 2007

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“…Similar conclusions for MDA-MB-231 cells have been recently suggested (Suarez-Cuervo et al, 2004). In addition to above-mentioned mechanisms, recent studies have suggested that MMP-9 may promote tumor angiogenesis by recruiting pericytes along vascular endothelial cells (Chantrain et al, 2004), via a release of soluble c-kit ligand (Heissig et al, 2002), and by recruiting bone marrow-derived precursor cells to the tumor stroma (Jodele et al, 2005). Thus, multiple mechanisms may operate downstream of TGF-b-ALK5 signaling to enhance tumor angiogenesis and our results indicate that MMP-9 is a critical component of this program.…”

Section: Discussionsupporting

confidence: 81%

“…Although it is well documented that MMP-9 is required for tumor progression (Bergers et al, 2000;Welch et al, 2000), the source of MMP-9 is still a subject of discussion. It has been shown that MMP-9 is secreted by tumor cells (Farina et al, 1998;Janji et al, 1999;Suarez-Cuervo et al, 2004) as well as by cells residing in stromal compartments (Chantrain et al, 2004;Jodele et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

ALK5 promotes tumor angiogenesis by upregulating matrix metalloproteinase-9 in tumor cells

2006

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Transforming growth factor beta 1 (TGF-b1) is a potent tumor suppressor but, paradoxically, TGF-b1 enhances tumor growth and metastasis in the late stages of cancer progression. This study investigated the role of TGF-b type I receptor, ALK5, and three mitogen-activated protein kinases (MAPKs) in metastasis by breast cancer cell line MDA-MB-231. We show that autocrine TGF-b signaling in MDA-MB-231 cells is required for tumor cell invasion and tumor angiogenesis. Expression of kinaseinactive ALK5 reduces tumor invasion and formation of new blood vessels within the tumor orthotopic xenografts in severe combined immunodeficiency (SCID) mice. In contrast, constitutively active ALK5-T204D enhances tumor invasion and angiogenesis by stimulating expression of matrix metalloproteinase MMP-9/gelatinase-B. Ablation of MMP-9 in ALK5-T204D cells by RNA interference (RNAi) reduces tumor invasion and tumor growth. Importantly, RNAi-MMP-9 reduces tumor neovasculature and increases tumor cell death. Induction of MMP-9 by TGF-b-ALK5 signaling requires MEK-ERK but not JNK, p38 MAPK or Smad4. Dominant-negative MEK blocks and constitutively active MEK1 enhances MMP-9 expression. However, all three MAPK cascades (ERK, JNK and p38 MAPK) are required for TGF-b-mediated cell migration. Collectively, our results show that TGF-b-ALK5-MAPK signaling in tumor cells promotes tumor angiogenesis and MMP-9 is an important component of this program.

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“…MMP9 and MMP14 have another effect on the vasculature: the perivascular (or smooth muscle) cells that ensheath the endothelial cells of the blood vessels are missing or their density is significantly decreased in normal vessels and during tumour neoangiogenesis [57][58][59] . This defect is especially evident in the smaller arterioles of the brain, and many of the remaining perivascular cells have irregular morphology.…”

Section: Mmps In Blood-vessel Remodellingmentioning

confidence: 99%

Matrix metalloproteinases and the regulation of tissue remodelling

Page-McCaw

Ewald

Werb

2007

Nat Rev Mol Cell Biol

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2,560

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Matrix metalloproteinases (MMPs) were discovered because of their role in amphibian metamorphosis, yet they have attracted more attention because of their roles in disease. Despite intensive scrutiny in vitro, in cell culture and in animal models, the normal physiological roles of these extracellular proteases have been elusive. Recent studies in mice and flies point to essential roles of MMPs as mediators of change and physical adaptation in tissues, whether developmentally regulated, environmentally induced or disease associated.The founding member of the matrix metalloproteinase (MMP) family, collagenase, was identified in 1962 by Gross and Lapiere, who found that tadpole tails during metamorphosis contained an enzyme that could degrade fibrillar collagen 1,2 . Subsequently, an interstitial collagenase, collagenase-1 or MMP1, was found in diseased skin and synovium 3 . In vitro, MMP1 initiates degradation of native fibrillar collagens, crucial components of vertebrate extracellular matrix (ECM), by cleaving the peptide bond between Gly775-Ile776 or Gly775-Lys776 in native type I, II or III collagen molecules 3,4 . Further research led to the discovery of a family of structurally related proteinases (23 in human, 24 in mice), now referred to as the MMP family.Interest in MMPs increased in the late 1960s and early 1970s following observations that MMPs are upregulated in diverse human diseases including rheumatoid arthritis and cancer. Importantly, high levels of MMPs often correlated with poor prognosis in human patients (reviewed in REF. 5 ). However, recent clinical data indicate that the relationship between § These authors contributed equally to this paper. Competing interests statementThe authors declare no competing financial interests. DATABASESThe following terms in this article are linked online to: Entrez Genome: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene DmMmp1 | DmMmp2 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptMMPs and disease is not simple; for example, increased MMP activity can enhance tumour progression or can inhibit it (reviewed in REF. 6 ). This complex relationship between MMP expression and cancer has increased the basic and clinical interest in understanding MMP function in vivo, but it has also focused attention on MMPs and pathology, and relatively less attention has been focused on the normal roles of these enzymes. MMP proteolysisMMPs are members of the metzincin group of proteases, which are named after the zinc ion and the conserved Met residue at the active site 11,12 . Recent work has generated a unified peptidase nomenclature 13 Functions of MMP proteolysisHistorically, MMPs were thought to function mainly as enzymes that degrade structural components of the ECM. However, MMP proteolysis can create space for cells to migrate, can produce specific substrate-cleavage fragments with independent biological activity, can MMPs in bone modelling and remodellingBone is an important site of ongoing tissue remodelling during development...

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Stromal Matrix Metalloproteinase-9 Regulates the Vascular Architecture in Neuroblastoma by Promoting Pericyte Recruitment

Cited by 199 publications

References 46 publications

Study of matrix metalloproteinases and their inhibitors in breast cancer

Study of matrix metalloproteinases and their inhibitors in breast cancer

ALK5 promotes tumor angiogenesis by upregulating matrix metalloproteinase-9 in tumor cells

Matrix metalloproteinases and the regulation of tissue remodelling

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