Role of tenascins in the ECM of gliomas

Brösicke, Nicole; Faissner, Andréas

doi:10.1080/19336918.2014.1000071

Cited by 83 publications

(60 citation statements)

References 154 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tenascins are very large multimeric glycoproteins that are mainly expressed during embryonic development, downregulated in adults, and re‐expressed under pathological conditions (Brosicke & Faissner, ; Imanaka‐Yoshida & Aoki, ). TN‐C consists of six polypeptide monomers, which are combined into the hexamer at their N‐termini (Erickson & Inglesias, ).…”

Section: The Brain Extracellular Matrix and Its Interaction With Gliomentioning

confidence: 99%

Glioma infiltration and extracellular matrix: key players and modulators

Ferrer

Moura‐Neto

Mentlein

2018

Glia

155

View full text Add to dashboard Cite

An outstanding characteristic of gliomas is their infiltration into brain parenchyma, a property that impairs complete surgical resection; consequently, these tumors might recur, resulting in a high mortality rate. Gliomas invade along preferential routes, such as those along white matter tracts and in the perineuronal and perivascular spaces. Brain extracellular components and their partners and modulators play a crucial role in glioma cell invasion. This review presents an extensive survey of the literature, showing how the brain extracellular matrix (ECM) is modulated during the glioma infiltration process. We explore aspects of ECM interaction with glioma cells, reviewing the main glycosaminoglycans, glycoproteins and proteoglycans. We discuss the roles of ECM-binding proteins, including CD44, RHAMM, integrins and axonal guidance molecules, and highlight the role of proteases and glycosidases in glioma infiltration; in binding and release chemokines, cytokines and growth factors; and in generating new bioactive ECM fragments. We also consider the roles of cytoskeletal signaling, angiogenesis, miRNAs and the glial-to-mesenchymal transition linked to glioma invasion. We closely discuss therapeutic approaches based on the modulation of the extracellular matrix, targeting the control of glioma infiltration, its relative failure in clinical trials, and potential means to overcome this difficulty.

show abstract

Section: The Brain Extracellular Matrix and Its Interaction With Gliomentioning

confidence: 99%

Glioma infiltration and extracellular matrix: key players and modulators

Ferrer

Moura‐Neto

Mentlein

2018

Glia

155

View full text Add to dashboard Cite

show abstract

“…These macromolecules can serve as a reservoir for heparin-binding angiogenic growth factors, such as fibroblast growth factors (FGFs) and VEGFs, which are subsequently released in a localized manner by heparanase (Kundu et al, 2016). Vessel-associated macromolecules, which are upregulated on the glioma vasculature include tenascin C (TNC) and periostin (Brosicke and Faissner, 2015; Mustafa et al, 2012), which interestingly are also critical niche factors for promoting cancer cell survival (Oskarsson et al, 2014). Moreover, periostin can be secreted by glioma stem cells to promote recruitment of tumor-promoting M2-like macrophage progenitors from the peripheral circulation (Zhou et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

The Microenvironmental Landscape of Brain Tumors

2017

View full text Add to dashboard Cite

The brain tumor microenvironment (TME) is emerging as a critical regulator of cancer progression in primary and metastatic brain malignancies. The unique properties of this organ require a specific framework for designing TME-targeted interventions. Here we discuss a number of these distinct features, including brain-resident cell types, the blood-brain barrier, and various aspects of the immune-suppressive environment. We also highlight recent advances in therapeutically targeting the brain TME in cancer. By developing a comprehensive understanding of the complex and interconnected microenvironmental landscape of brain malignancies we will greatly expand the range of therapeutic strategies available to target these deadly diseases.

show abstract

“…Invasion-promoting ECM glycoproteins secreted in glioma are: Secreted Protein Acidic and Rich in Cysteine (SPARC); TN-C supporting cell adhesion through integrin binding; OPN and VN (87)(88)(89)(90). In addition, TSP-1, a multifunctional matrix glycoprotein, is implicated in cell adhesion, migration, invasion, and activation of TGF-β (91; see the section "The Role of TGF-β in Glioma Cell Motility").…”

Section: Chondroitin Sulfate Proteoglycans Glycoproteins and Galectinsmentioning

confidence: 99%

Molecular Mechanisms of Glioma Cell Motility

et al. 2017

View full text Add to dashboard Cite

Gliomas are the most common intracranial tumors in humans. The most malignant among these tumors is glioblastoma (GBM), with an incidence of 3-5 out of 100,000 persons in Western countries. GBM arises either de novo (primary GBM) or develops from a lower grade glioma (secondary GBM). The prognosis is poor. GBMs are lethal tumors and even optimal surgical resection, followed by chemotherapy and irradiation, results in a median survival of about 12-15 months. One characteristic that is responsible for GBM malignancy, and its worse prognosis, is the highly infiltrative growth of GBM cells into the healthy brain. GBM cell migration and invasion is a very complex process that is regulated by several factors, which include changes in the migrating cell itself as well as the tumor microenvironment. This chapter provides an overview of routes of invasion of glioma cells, the signaling pathways that drive glioma cell motility, and the processes through which glioma cells modulate their surrounding environment.

show abstract

Role of tenascins in the ECM of gliomas

Cited by 83 publications

References 154 publications

Glioma infiltration and extracellular matrix: key players and modulators

Glioma infiltration and extracellular matrix: key players and modulators

The Microenvironmental Landscape of Brain Tumors

Molecular Mechanisms of Glioma Cell Motility

Contact Info

Product

Resources

About