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Merzak, Abderrahim; Pilkington, Geoffrey J.

doi:10.1023/a:1005760726850

Cited by 32 publications

(8 citation statements)

References 177 publications

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“…Additive Effects of Aggrecanase-1 and MMP-2 on Brevican Digestion-Among MMP-1, -2, -3, -7, -8, -10, and -13, capable of digesting brevican, only MMP-2 is so far known to be expressed and also activated in human gliomas (17,29). In addition, our preliminary study showed that aggrecanase-1 is expressed in gliomas as well as in normal human brain tissues.…”

Section: Resultsmentioning

confidence: 70%

“…Thus, the disruption or weakening of the brevican-hyaluronan and/or brevican-tenascin-R interactions may be one of the factors that accelerate the invasiveness of glioma cells. Such disruption can be induced by cleavage of the brevican core proteins by aggrecanase-1 and/or MMP-2, both of which are present in human glioma tissues (17,29). 2 These hypotheses remain to be elucidated by further studies of how the brevican fragments generated by the action of the MMPs and/or aggrecanase-1 affect glioma cell invasion.…”

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confidence: 99%

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Brevican Is Degraded by Matrix Metalloproteinases and Aggrecanase-1 (ADAMTS4) at Different Sites

Nakamura¹,

Fujii²,

Inoki³

et al. 2000

Journal of Biological Chemistry

157

131

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Brevican is a member of the lectican family of chondroitin sulfate proteoglycans that is predominantly expressed in the central nervous system. The susceptibility of brevican to digestion by matrix metalloproteinases (MMP-1, -2, -3, -7, -8, -9, -10, and -13 and membrane type 1 and 3 MMPs) and aggrecanase-1 (ADAMTS4) was examined. MMP-1, -2, -3, -7, -8, -10, and -13 degraded brevican into a few fragments with similar molecular masses, whereas the degradation products of aggrecanase-1 had apparently different sizes. NH 2 -terminal sequence analyses of the digestion fragments revealed that cleavages of the brevican core protein by these metalloproteinases occurred commonly within the central non-homologous domain. MMP-1, -2, -3, -7, -8, -10, and -13 preferentially attacked the Ala

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Section: Resultsmentioning

confidence: 70%

mentioning

confidence: 99%

Brevican Is Degraded by Matrix Metalloproteinases and Aggrecanase-1 (ADAMTS4) at Different Sites

Nakamura¹,

Fujii²,

Inoki³

et al. 2000

Journal of Biological Chemistry

157

131

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“…Previous studies have also revealed the co-localisation of CD155 with integrin subunit especially α v and β 3 , known to mediate focal adhesion by forming physical transmembrane link between ECM and the underlying cytoskeleton elements [4], [41]. Therefore, CD155 expressed at the cell periphery and filopodia of migrating cells may be associated with adhesion and directional motility [20].…”

Section: Discussionmentioning

confidence: 97%

Receptors for Hyaluronic Acid and Poliovirus: A Combinatorial Role in Glioma Invasion?

Maherally

Smith²,

An³

et al. 2012

PLoS ONE

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BackgroundCD44 has long been associated with glioma invasion while, more recently, CD155 has been implicated in playing a similar role. Notably, these two receptors have been shown closely positioned on monocytes.Methods and FindingsIn this study, an up-regulation of CD44 and CD155 was demonstrated in established and early-passage cultures of glioblastoma. Total internal reflected fluorescence (TIRF) microscopy revealed close proximity of CD44 and CD155. CD44 antibody blocking and gene silencing (via siRNA) resulted in greater inhibition of invasion than that for CD155. Combined interference resulted in 86% inhibition of invasion, although in these investigations no obvious evidence of synergy between CD44 and CD155 in curbing invasion was shown. Both siRNA-CD44 and siRNA-CD155 treated cells lacked processes and were rounder, while live cell imaging showed reduced motility rate compared to wild type cells. Adhesion assay demonstrated that wild type cells adhered most efficiently to laminin, whereas siRNA-treated cells (p<0.0001 for both CD44 and CD155 expression) showed decreased adhesion on several ECMs investigated. BrdU assay showed a higher proliferation of siRNA-CD44 and siRNA-CD155 cells, inversely correlated with reduced invasion. Confocal microscopy revealed overlapping of CD155 and integrins (β1, αvβ1 and αvβ3) on glioblastoma cell processes whereas siRNA-transfected cells showed consequent reduction in integrin expression with no specific staining patterns. Reduced expression of Rho GTPases, Cdc42, Rac1/2/3, RhoA and RhoB, was seen in siRNA-CD44 and siRNA-CD155 cells. In contrast to CD44-knockdown and ‘double’-knockdown cells, no obvious decrease in RhoC expression was observed in CD155-knockdown cells.ConclusionsThis investigation has enhanced our understanding of cell invasion and confirmed CD44 to play a more significant role in this biological process than CD155. Joint CD44/CD155 approaches may, however, merit further study in therapeutic targeting of infiltrating glioma cells.

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“…[1][2][3] Conventional clinical approaches rely (HA) is the main extracellular matrix component of brain tissue also believed to alter glioblastoma invasive phenotype. [9][10][11][12] As a result, the main cell surface receptor for HA, CD44 is thought to play an important role in altering GBM invasion via direct CD44-HA interactions. [10] A number of studies have begun to explore the use of in vitro platforms to quantify glioblastoma invasion.…”

Section: Introductionmentioning

confidence: 99%

The Combined Influence of Hydrogel Stiffness and Matrix‐Bound Hyaluronic Acid Content on Glioblastoma Invasion

Chen

Pedrón

Harley

2017

Macromolecular Bioscience

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Glioblastoma (GBM) is the most common and lethal form of brain cancer. Its high mortality is associated with its aggressive invasion throughout the brain. The heterogeneity of stiffness and hyaluronic acid (HA) content within the brain makes it difficult to study invasion in vivo. A dextran-bead assay is employed to quantify GBM invasion within HA-functionalized gelatin hydrogels. Using a library of stiffness-matched hydrogels with variable levels of matrix-bound HA, it is reported that U251 GBM invasion is enhanced in softer hydrogels but reduced in the presence of matrix-bound HA. Inhibiting HA–CD44 interactions reduces invasion, even in hydrogels lacking matrix-bound HA. Analysis of HA biosynthesis suggests that GBM cells compensate for a lack of matrix-bound HA by producing soluble HA to stimulate invasion. Together, a robust method is showed to quantify GBM invasion over long culture times to reveal the coordinated effect of matrix stiffness, immobilized HA, and compensatory HA production on GBM invasion.

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Cited by 32 publications

References 177 publications

Brevican Is Degraded by Matrix Metalloproteinases and Aggrecanase-1 (ADAMTS4) at Different Sites

Brevican Is Degraded by Matrix Metalloproteinases and Aggrecanase-1 (ADAMTS4) at Different Sites

Receptors for Hyaluronic Acid and Poliovirus: A Combinatorial Role in Glioma Invasion?

The Combined Influence of Hydrogel Stiffness and Matrix‐Bound Hyaluronic Acid Content on Glioblastoma Invasion

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