Cleavage of Lumican by Membrane-Type Matrix Metalloproteinase-1 Abrogates This Proteoglycan-Mediated Suppression of Tumor Cell Colony Formation in Soft Agar

Li, Yingyi; Aoki, Takanori; Mori, Yusuke; Ahmad, Munirah; Miyamori, Hisashi; Takino, Takahisa; Sato, Hiroshi

doi:10.1158/0008-5472.can-04-1038

Cited by 99 publications

(96 citation statements)

References 50 publications

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“…In addition, MT1-MMP cleaves extracellular matrix and cell adhesion signaling receptors and tumor suppressor proteins, including type I collagen, lumican, laminin, tissue transglutaminase, CD44, integrins, LRP, gC1Q-R/p33, and KiSS 1 (18,42,(46)(47)(48)(49)(50)(51). We have also determined that MT1-MMP interacts with the C1q and C3b components of the complement system and inactivates the complement propagation cascade.…”

Section: Discussionmentioning

confidence: 90%

Interference with the Complement System by Tumor Cell Membrane Type-1 Matrix Metalloproteinase Plays a Significant Role in Promoting Metastasis in Mice

Rozanov¹,

Savinov²,

Golubkov³

et al. 2006

Cancer Research

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Neoplasms have developed strategies to protect themselves against the complement-mediated host immunity. Invasionand metastasis-promoting membrane type-1 (MT1) matrix metalloproteinase (MMP) is strongly associated with many metastatic cancer types. The relative importance of the individual functions of MT1-MMP in metastasis was, however, unknown. We have now determined that the expression of murine MT1-MMP in murine melanoma B16F1 cells strongly increased the number of metastatic loci in the lungs of syngeneic C57BL/6 mice. In contrast, MT1-MMP did not affect the number of metastatic loci in complement-deficient C57BL/6-C3 À/À mice. Our results indicated, for the first time, that the anticomplement activity of MT1-MMP played a significant role in promoting metastasis in vivo and determined the relative importance of the anticomplement activity in the total metastatic effect of this multifunctional proteolytic enzyme. We believe that our results shed additional light on the functions of MT1-MMP in cancer and clearly make this protease a promising drug target in metastatic malignancies.

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Section: Discussionmentioning

confidence: 90%

Interference with the Complement System by Tumor Cell Membrane Type-1 Matrix Metalloproteinase Plays a Significant Role in Promoting Metastasis in Mice

Rozanov¹,

Savinov²,

Golubkov³

et al. 2006

Cancer Research

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“…Sp1 regulates and interacts with a number of other transcription factors, including Smad, which regulates TGF␤1 signaling (21,37). Sp1 can also regulate collagen and lumican gene transcription (38), both of which were overexpressed in FF mice. We therefore looked at gene expression levels of Sp1 in these groups of mice.…”

Section: Animals Reared On the Ff Diet Recapitulate The Clinical Phenmentioning

confidence: 99%

Fast food diet mouse: novel small animal model of NASH with ballooning, progressive fibrosis, and high physiological fidelity to the human condition

Charlton

Krishnan

Viker

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

388

354

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Although there are small animal platforms that recapitulate some of the histological features of nonalcoholic fatty liver disease, there are no small animal models of nonalcoholic steatohepatitis (NASH) with consistent hepatocellular ballooning and progressive fibrosis that also exhibit fidelity to the human condition physiologically. We examined the metabolic and histological effects of a diet on the basis of the composition of “fast food” (high saturated fats, cholesterol, and fructose). Mice ( n = 8 in each group) were assigned to diets as follows: 1) standard chow (SC), i.e., 13% energy as fat [1% saturated fatty acids (SFA)], 2) high fat (HF), i.e., 60% energy as fat (1% SFA), and 3) fast food (FF), i.e., 40% energy as fat (12% SFA, 2% cholesterol). All three diets were supplemented with high fructose. All diets produced obesity. The HF and FF diets produced insulin resistance. Liver histology was normal in animals fed the SC diet. Steatohepatitis with pronounced ballooning and progressive fibrosis (stage 2) was observed in mice fed the FF diet. Although the HF diet produced obesity, insulin resistance, and some steatosis; inflammation was minimal, and there was no increase in fibrosis. The FF diet produced a gene expression signature of increased fibrosis, inflammation, and endoplasmic reticulum stress and lipoapoptosis. A diet based on high cholesterol, high saturated fat, and high fructose recapitulates features of the metabolic syndrome and NASH with progressive fibrosis. This represents a novel small animal model of fibrosing NASH with high fidelity to the human condition. These results highlight the contribution of dietary composition to the development of nonalcoholic fatty liver disease and NASH.

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“…161 Interestingly, both lumican and decorin can be cleaved by MMP-1, suggesting that proteolytic processing is very precisely regulated and crucial for proteoglycan-mediated spatiotemporal functions. 162 Like biglycan and decorin, lumican is also important in modulating the inflammatory response by presenting lipopolysaccharide to CD14, thereby activating TLR-4 in macrophages. 163 Furthermore, lumican regulates neutrophil infiltration in a murine keratitis model, by interacting with CXCL1, thus creating a chemokine gradient along which these neutrophils infiltrate the injured tissue.…”

Section: Class II Slrps: Lumicanmentioning

confidence: 99%

Myocardial Extracellular Matrix

Rienks

Papageorgiou

Frangogiannis

et al. 2014

Circulation Research

314

170

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Abstract:The cardiac extracellular matrix (ECM) is a complex architectural network consisting of structural and nonstructural proteins, creating strength and plasticity. The nonstructural compartment of the ECM houses a variety of proteins, which are vital for ECM plasticity, and can be divided into 3 major groups: glycoproteins, proteoglycans, and glycosaminoglycans. The common denominator for these groups is glycosylation, which refers to the decoration of proteins or lipids with sugars. This review will discuss the fundamental role of the matrix in cardiac development, homeostasis, and remodeling, from a glycobiology point of view. Glycoproteins (eg, thrombospondins, secreted protein acidic and rich in cysteine, tenascins), proteoglycans (eg, versican, syndecans, biglycan), and glycosaminoglycans (eg, hyaluronan, heparan sulfate) are upregulated on cardiac injury and regulate key processes in the remodeling myocardium such as inflammation, fibrosis, and angiogenesis. Albeit some parallels can be made regarding the processes these proteins are involved in, their specific functions are extremely diverse. In fact, under varying conditions, individual proteins can even have opposing functions, making spatiotemporal contribution of these proteins in the rearrangement of multifaceted ECM very hard to grasp. Alterations of protein characteristics by the addition of sugars may explain the immense, yet tightly regulated, variability of the remodeling cardiac matrix. Understanding the role of glycosylation in altering the ultimate function of glycoproteins, proteoglycans, and glycosaminoglycans in the myocardium may lead to the development of new biochemical structures or compounds with great therapeutic potential for patients with heart disease. (Circ Res. 2014;114:872-888.)

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Cleavage of Lumican by Membrane-Type Matrix Metalloproteinase-1 Abrogates This Proteoglycan-Mediated Suppression of Tumor Cell Colony Formation in Soft Agar

Abstract: The small leucine-rich proteoglycan lumican was identified from a human placenta cDNA library by the expression cloning method as a gene product that interacts with membrane-type matrix metalloproteinase-1 (

Cited by 99 publications

References 50 publications

Interference with the Complement System by Tumor Cell Membrane Type-1 Matrix Metalloproteinase Plays a Significant Role in Promoting Metastasis in Mice

Interference with the Complement System by Tumor Cell Membrane Type-1 Matrix Metalloproteinase Plays a Significant Role in Promoting Metastasis in Mice

Fast food diet mouse: novel small animal model of NASH with ballooning, progressive fibrosis, and high physiological fidelity to the human condition

Myocardial Extracellular Matrix

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