Tenascin-C and carcinoma cell invasion in oral and urinary bladder cancer

Berndt, Alexander; Richter, Petra; Kosmehl, Hartwig; Franz, Marcus

doi:10.1080/19336918.2015.1005463

Cited by 30 publications

(26 citation statements)

References 86 publications

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“…Heparanase, an important modulator of ECM, through its heparin and heparan sulfate cleaving effects, was found to influence both FGF and TGF‐β‐dependent EMT (Masola et al, , ). Furthermore, PDGF through regulating tenascin‐C expression modulates ECM reorganization and EMT in bladder cancer (Berndt et al, ).…”

Section: Discussionmentioning

confidence: 99%

Role of the extracellular matrix in cancer‐associated epithelial to mesenchymal transition phenomenon

Tzanakakis

Kavasi

Voudouri

et al. 2017

Developmental Dynamics

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The epithelial to mesenchymal transition (EMT) program is a crucial component in the processes of morphogenesis and embryonic development. The transition of epithelial to mesenchymal phenotype is associated with numerous structural and functional changes, including loss of cell polarity and tight cell-cell junctions, the acquisition of invasive abilities, and the expression of mesenchymal proteins. The switch between the two phenotypes is involved in human pathology and is crucial for cancer progression. Extracellular matrices (ECMs) are multi-component networks that surround cells in tissues. These networks are obligatory for cell survival, growth, and differentiation as well as tissue organization. Indeed, the ECM suprastructure, in addition to its supportive role, can process and deliver a plethora of signals to cells, which ultimately regulate their behavior. Importantly, the ECM derived signals are critically involved in the process of EMT during tumorigenesis. This review discusses the multilayer interaction between the ECM and the EMT process, focusing on contributions of discrete mediators, a strategy that may identify novel potential target molecules. Developmental Dynamics 247:368-381, 2018. V C 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Role of the extracellular matrix in cancer‐associated epithelial to mesenchymal transition phenomenon

Tzanakakis

Kavasi

Voudouri

et al. 2017

Developmental Dynamics

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“…In addition, isoforms of TN-C generated via alternative splicing have shown functional heterogeneity that includes effects on cell proliferation and migration. Thus far, TN-C has been implicated in various diseases including cancers and sarcomas, fibrosis, and cardiovascular disease (124–127). TN-R, TN-W, and TN-X exist in multiple isoforms and are less well studied with limited reports linking them to vascular calcification, Ehlers-Danlos syndrome, and CNS diseases (128–131).…”

Section: Introductionmentioning

confidence: 99%

Matricellular proteins in drug delivery: Therapeutic targets, active agents, and therapeutic localization

Sawyer

Kyriakides

2016

Advanced Drug Delivery Reviews

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Extracellular matrix is composed by a complex array of molecules that together provide structural and functional support to cells. These properties are mainly mediated by the activity of collagenous and elastic fibers, proteoglycans, and proteins such as fibronectin and laminin. ECM composition is tissue-specific and could include matricellular proteins whose primary role is to modulate cell-matrix interactions. In adults, matricellular proteins are primarily expressed during injury, inflammation and disease. Particularly, they are closely associated with the progression and prognosis of cardiovascular and fibrotic diseases, and cancer. This review aims to provide an overview of the potential use of matricellular proteins in drug delivery including the generation of therapeutic agents based on the properties and structures of these proteins as well as their utility as biomarkers for specific diseases.

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“…However, prominent de novo expression of TNC is reported in the adult tissues in various pathophysiologic conditions, such as tissue injury/wound healing, inflammation, and tumorigenesis. [11][12][13] As a so-called matricellular protein, TNC is not an obligatory structural element in the ECM, but it is able to bind to ECM structural proteins and cell surface receptors such as the EGF receptor (EGFR) and integrins. 8,14,15 TNC binding to these receptors causes activation of their downstream pathways, thereby modulating cell adhesion, spreading, migration, and proliferation in a cell type-and context-dependent manner.…”

mentioning

confidence: 99%

Tenascin-C Is a Major Component of the Fibrogenic Niche in Kidney Fibrosis

Tian

Zhou

et al. 2016

JASN

101

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Kidney fibrosis initiates at certain focal sites in which the fibrogenic niche provides a specialized microenvironment that facilitates fibroblast activation and proliferation. However, the molecular identity of these fibrogenic niches is poorly characterized. Here, we determined whether tenascin-C (TNC), an extracellular matrix glycoprotein, is a component of the fibrogenic niche in kidney fibrosis. , TNC expression increased rapidly in kidneys subjected to unilateral ureteral obstruction or ischemia/reperfusion injury and predominantly localized at the foci rich in fibroblasts in renal interstitium., TNC selectively promoted renal interstitial fibroblast proliferation, bromodeoxyuridine incorporation, and the expression of proliferation-related genes. The mitogenic activity of TNC required the integrin/focal adhesion kinase/mitogen-activated protein kinase signaling cascade. Using decellularized extracellular matrix scaffolds, we found that TNC-enriched scaffolds facilitated fibroblast proliferation, whereas TNC-deprived scaffolds inhibited proliferation. Matrix scaffold prepared from fibrotic kidney also promoted greater fibroblast proliferation than did scaffolds prepared from healthy kidney. Conversely, small interfering RNA-mediated knockdown of TNC repressed injury-induced fibroblast expansion and renal fibrosis. These studies identify TNC as a major constituent of the fibrogenic niche that promotes fibroblast proliferation, and illustrate a pivotal role for the TNC-enriched microenvironment in kidney fibrogenesis.

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Tenascin-C and carcinoma cell invasion in oral and urinary bladder cancer

Cited by 30 publications

References 86 publications

Role of the extracellular matrix in cancer‐associated epithelial to mesenchymal transition phenomenon

Role of the extracellular matrix in cancer‐associated epithelial to mesenchymal transition phenomenon

Matricellular proteins in drug delivery: Therapeutic targets, active agents, and therapeutic localization

Tenascin-C Is a Major Component of the Fibrogenic Niche in Kidney Fibrosis

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