Angiogenesis and tumour progression: migration-stimulating factor as a novel target for clinical intervention

Schor, Ana M.; Schor, Seth L.

doi:10.1038/eye.2009.314

Cited by 19 publications

(17 citation statements)

References 42 publications

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“…MSF message and protein are also expressed by tumour cells and associated stromal fibroblasts and endothelial cells in >80% of human cancers examined to date, including common carcinomas, melanomas and gliomas. In agreement with previous in vitro studies, recent immunohistochemical data confirm that MSF protein may also be expressed by skin cells at distant uninvolved sites in cancer patients (Refs 2–4,13,. unpublished observations).…”

supporting

confidence: 91%

Bistable switch in migration stimulating factor expression: Regulation by the concerted signalling of transforming growth factor‐β1 and the extracellular matrix

Schor

Ellis

Jones

et al. 2011

Intl Journal of Cancer

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Migration stimulating factor (MSF) is an oncofetal motogenic/angiogenic cytokine constitutively expressed by epithelial and stromal cells in fetal and neoplastic tissues. Fibroblasts derived from healthy adult skin do not express MSF but can be induced to do so by treatment with transforming growth factor-b1 (TGF-b1). As the bioactivities of both MSF and TGF-b1 are modulated by the extracellular matrix, we investigated whether the induction of MSF expression by TGF-b1 is also matrix dependent. We now report that adult fibroblasts are induced to express MSF by a transient treatment with TGF-b1 (as short as 2 hr) but only when the cells are adherent to a ''wound'' matrix, such as denatured type I collagen, fibrin or plastic tissue culture dishes. Unexpectedly, this induction of MSF expression persists unabated for the entire subsequent lifespan of the treated cells in the absence of further TGF-b1 and irrespective of the substratum. Such ''activated'' MSF expression may, however, be persistently switched off again by a second transient exposure to TGF-b1 but this time only when the cells are adherent to a ''healthy'' matrix of native type I collagen. Significantly, the constitutive expression of MSF by fetal and cancer patient fibroblasts could also be persistently switched off by this means. We conclude that TGF-b1 may both switch on and switch off MSF expression in a manner critically determined by the nature of the matrix substratum and suggest that this may be a possible mechanism underlying the observed dual functionality of TGF-b1 as both a tumour suppressor and tumour promoter.Migration stimulating factor (MSF) is a motogenic and angiogenic cytokine exhibiting an oncofetal expression profile. [1][2][3][4][5] Skin fibroblasts derived from more than 90% of healthy adults do not express MSF and display a low baseline level of migration into three-dimensional (3D) gels of native type I collagen fibres. In contrast, more than 90% of fetal fibroblasts and 50-90% of cancer patient fibroblasts express MSF and consequently migrate to a significantly greater extent than do their healthy adult-derived counterparts. Although not expressing MSF, healthy adult fibroblasts remain responsive to it, as evidenced by the stimulation of their migration by either recombinant human MSF (rhMSF) or conditioned medium (CM) from fetal or cancer patient fibroblasts. 1,[6][7][8][9] MSF is a genetically truncated isoform of fibronectin. 2 Approximately 20 ''full-length'' fibronectin isoforms had been identified when MSF was cloned, all of which consisted of two peptide chains (250-280 kDa each) covalently linked by disulfide bonds at their respective C-termini. 10 In contrast, MSF (with a molecular mass of 70 kDa) is a soluble single chain protein identical to the N-terminus of the fibronectin monomer up to and including the amino acid sequence coded by exon III-1a (Fig. 1a). MSF expression by fibroblasts is controlled by a two-step process in which the primary fibronectin gene transcript is foreshortened as a result of read-through of...

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supporting

confidence: 91%

Bistable switch in migration stimulating factor expression: Regulation by the concerted signalling of transforming growth factor‐β1 and the extracellular matrix

Schor

Ellis

Jones

et al. 2011

Intl Journal of Cancer

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“…Among other functions, MSF constitute an autocrine survival factor for the angiogenic endothelium, while a significant association between elevated MSF expression and poor cancer patients' survival has been noticed [30].…”

Section: Assessment Of Tumor Angiogenesismentioning

confidence: 99%

Angiogenesis in salivary gland tumors: from clinical significance to treatment

Theocharis

Gribilas

Giaginis

et al. 2015

Expert Opinion on Therapeutic Targets

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The available data suggest that microvessel density (MVD) evaluation may be capable of discriminating between benign and malignant SGTs, while the use of CD105 antibody seems to be the most suitable. Substantial evidence also suggests that MVD and VEGF expression could be used as prognostic factors in malignant SGTs. Although several agents have shown antiangiogenic activities in adenoid cystic carcinoma cells and xenograft tumors, limited effectiveness in the existing clinical trials was noted. Further studies are strongly recommended for the validation of already well-known and the identification of novel prognostic and predictive angiogenic markers. There is also a strong demand for relatively larger cohorts, homogenous samples referring to same histological SGT subtypes and including an equivalent number of low- and high-grade SGTs.

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“…MSF displays a number of highly potent bioactivities, including the stimulation of normal and neoplastic cell migration, matrix remodeling and angiogenesis [7,[9][10][11][12]. Taken together with its oncofetal pattern of expression, this spectrum of bioactivities suggests that MSF may contribute to tumour progression.…”

Section: Introductionmentioning

confidence: 99%

“…MSF is an oncofetal regulatory protein constitutively expressed by a variety of cell types during fetal development, not expressed by the majority of cells in the healthy adult, but persistently re-expressed by both carcinoma and associated stromal cells in patients with breast and other human cancers [6][7][8][9][10][11][12]. MSF is a 70 kDa genetically truncated isoform of fibronectin [7].…”

Section: Introductionmentioning

confidence: 99%

Migration Stimulating Factor (MSF): A Novel Biomarker of Breast Cancer Progression

Perrier¹,

Woolston²,

Purdie³

2012

Translational

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Migration Stimulating Factor (MSF) is a novel oncofetal biomarker previously identified in a number of human tumours. The aim of this study was to evaluate the possible association between MSF expression and disease progression in breast cancer. Archival breast tissues examined included malignant tumours (T; n=23), benign tumours or pathologies (B; n=8) and histologically normal breast from either reduction mammoplasties (NB; n=19) or from tumour patients (NB-T; n=18). Sections were stained with MSF-specific antibodies and assessed by consensus of 3-4 independent observers in terms of various MSF indices, which represented overall, epithelial and stromal MSF expression. MSF was heterogeneously expressed by epithelial and stromal cells, with significant inter-group quantitative differences in the sequence NB

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Angiogenesis and tumour progression: migration-stimulating factor as a novel target for clinical intervention

Abstract: Migration-stimulating factor (MSF), a soluble genetically truncated isoform of fibronectin, is a potent oncofoetal regulatory molecule. Its 2

Cited by 19 publications

References 42 publications

Bistable switch in migration stimulating factor expression: Regulation by the concerted signalling of transforming growth factor‐β1 and the extracellular matrix

Bistable switch in migration stimulating factor expression: Regulation by the concerted signalling of transforming growth factor‐β1 and the extracellular matrix

Angiogenesis in salivary gland tumors: from clinical significance to treatment

Migration Stimulating Factor (MSF): A Novel Biomarker of Breast Cancer Progression

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