Endogenous Matrix-Derived Inhibitors of Angiogenesis

Sund, Malin; Nyberg, Pia; Eikesdal, Hans Petter

doi:10.3390/ph3103021

Cited by 10 publications

(11 citation statements)

References 113 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MATN-1 is the newest member of the family of matrix-derived inhibitors of neovascularization. As is the case with thrombospondin-1 and -2 (39 -41), it distinguishes itself from other inhibitors in this family such as endostatin (42,43), tumstatin (44,45), arresten (46), and canstatin (47) in that these latter inhibitors are proteolytically processed products of larger, largely angiogenesisinert matrix proteins (48,49).…”

Section: Discussionmentioning

confidence: 99%

Matrilin-1 Is an Inhibitor of Neovascularization

Foradori

Chen

Fernández

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background:The relative avascularity of cartilage has made it a promising source of angiogenesis inhibitors. Results: MATN-1, identified by mass spectrometry, suppresses capillary endothelial cell proliferation and migration. Conclusion: MATN-1 is a novel inhibitor of neovascularization in vivo and in vitro.Significance: This is the first demonstration that MATN-1 is an inhibitor of both normal and pathological neovascularization.

show abstract

Section: Discussionmentioning

confidence: 99%

Matrilin-1 Is an Inhibitor of Neovascularization

Foradori

Chen

Fernández

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Matricryptins regulating angiogenesis and tumor growth target endothelial cells and/or tumor cells (Robinet et al, 2005 ; Tran et al, 2008 ; Sund et al, 2010 ; Boosani and Sudhakar, 2011 ; Ricard-Blum and Ballut, 2011 ; Toupance et al, 2012 ; Kikkawa et al, 2013 ; Monboisse et al, 2014 ; Ricard-Blum and Salza, 2014 ; Monslow et al, 2015 ; Nikitovic et al, 2015 ; Ricard-Blum and Vallet, 2015 ; Walia et al, 2015 ). Several matricryptins inhibit the proliferation and the migration of endothelial cells, block cell cycle at G1 as shown for anastellin (Ambesi et al, 2005 ) and endostatin (Hanai et al, 2002 ) and induce apoptosis.…”

Section: Regulation Of Angiogenesis Tumor Growth and Metastasis By Mmentioning

confidence: 99%

“…We have extended the definition of matricryptins to the ectodomains of membrane collagens and membrane proteoglycans, which are released in the ECM by sheddases, and to fragments of ECM-associated enzymes such as lysyl oxidase, which initiates the covalent cross-linking of collagens and elastin, and matrix metalloproteinases (MMPs), which contribute to ECM remodeling (Ricard-Blum and Salza, 2014 ; Ricard-Blum and Vallet, 2015 ). The molecular functions of matricryptins and the biological processes they regulate have been reviewed with a focus on collagen and proteoglycan matricryptins (Ricard-Blum and Ballut, 2011 ), on matricryptins regulating tissue repair (Ricard-Blum and Salza, 2014 ), angiogenesis (Sund et al, 2010 ; Boosani and Sudhakar, 2011 ; Gunda and Sudhakar, 2013 ), cancer (Monboisse et al, 2014 ), and on the proteases releasing matricryptins (Ricard-Blum and Vallet, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Matricryptins Network with Matricellular Receptors at the Surface of Endothelial and Tumor Cells

Ricard‐Blum

Vallet

2016

Front. Pharmacol.

View full text Add to dashboard Cite

The extracellular matrix (ECM) is a source of bioactive fragments called matricryptins or matrikines resulting from the proteolytic cleavage of extracellular proteins (e.g., collagens, elastin, and laminins) and proteoglycans (e.g., perlecan). Matrix metalloproteinases (MMPs), cathepsins, and bone-morphogenetic protein-1 release fragments, which regulate physiopathological processes including tumor growth, metastasis, and angiogenesis, a pre-requisite for tumor growth. A number of matricryptins, and/or synthetic peptides derived from them, are currently investigated as potential anti-cancer drugs both in vitro and in animal models. Modifications aiming at improving their efficiency and their delivery to their target cells are studied. However, their use as drugs is not straightforward. The biological activities of these fragments are mediated by several receptor families. Several matricryptins may bind to the same matricellular receptor, and a single matricryptin may bind to two different receptors belonging or not to the same family such as integrins and growth factor receptors. Furthermore, some matricryptins interact with each other, integrins and growth factor receptors crosstalk and a signaling pathway may be regulated by several matricryptins. This forms an intricate 3D interaction network at the surface of tumor and endothelial cells, which is tightly associated with other cell-surface associated molecules such as heparan sulfate, caveolin, and nucleolin. Deciphering the molecular mechanisms underlying the behavior of this network is required in order to optimize the development of matricryptins as anti-cancer agents.

show abstract

“…For example, both HIF-1α and VEGFR1 are critical inducers of angiogenesis, but their expression also mediates EMT [40,41]. To understand this regulation, we should be aware of two important subtleties: (1) proliferation and EMT are sometimes strikingly uncoupled, and (2) EMT activates matrix-metalloproteinases that cleaves extracellular-matrix components, such as type XVIII and IV collagen , to produce matrix-derived angiogenesis inhibitors [42]. I will to try to discuss the biological value of these observations.…”

Section: Invasion and Metastasis Include Distant Interactionsmentioning

confidence: 99%

An Evolutionary Explanation for the Perturbation of the Dynamics of Metastatic Tumors Induced by Surgery and Acute Inflammation

Carmona-Bayonas

2011

Cancers

View full text Add to dashboard Cite

Surgery has contributed to unveil a tumor behavior that is difficult to reconcile with the models of tumorigenesis based on gradualism. The postsurgical patterns of progression include unexpected features such as distant interactions and variable rhythms. The underlying evidence can be summarized as follows: (1) the resection of the primary tumor is able to accelerate the evolution of micrometastasis in early stages, and (2) the outcome is transiently opposed in advanced tumors. The objective of this paper is to give some insight into tumorigenesis and surgery-related effects, by applying the concepts of the evolutionary theory in those tumor behaviors that gompertzian and tissular-centered models are unable to explain. According to this view, tumors are the consequence of natural selection operating at the somatic level, which is the basic mechanism of tumorigenesis, notwithstanding the complementary role of the intrinsic constrictions of complex networks. A tumor is a complicated phenomenon that entails growth, evolution and development simultaneously. So, an evo-devo perspective can explain how and why tumor subclones are able to translate competition from a metabolic level into neoangiogenesis and the immune response. The paper proposes that distant interactions are an extension of the ecological events at the local level. This notion explains the evolutionary basis for tumor dormancy, and warns against the teleological view of tumorigenesis as a process directed towards the maximization of a concrete trait such as aggressiveness.

show abstract

Endogenous Matrix-Derived Inhibitors of Angiogenesis

Cited by 10 publications

References 113 publications

Matrilin-1 Is an Inhibitor of Neovascularization

Matrilin-1 Is an Inhibitor of Neovascularization

Matricryptins Network with Matricellular Receptors at the Surface of Endothelial and Tumor Cells

An Evolutionary Explanation for the Perturbation of the Dynamics of Metastatic Tumors Induced by Surgery and Acute Inflammation

Contact Info

Product

Resources

About