Tenascin: an extracellular matrix protein involved in tissue interactions during fetal development and oncogenesis

doi:10.1016/0092-8674(86)90374-0

Cell

Volume 47, Issue 1, 10 October 1986, Pages 131-139

https://doi.org/10.1016/0092-8674(86)90374-0 Get rights and content

Abstract

The extracellular matrix protein tenascin (previously described as myotendinous antigen) is selectively present in the mesenchyme surrouding fetal rat mammary glands, hair follicles, and teeth, three organ anlagen where the mesenchyme is essential for development. No tenascin is detectable in the normal adult mammary gland. Carcinogen-induced mammary tumors contained tenascin in their fibrous tissue. As reported for the molecule described as a “hexabrachion,” tenascin contaminates so-called “cell-surface fibronectin,” where it accounts for most of the detectable hemagglutinating activity. Of the extracellular matrix proteins compared, tenascin is the least effective substrate for attachment of primary mammary tumor cells, but the most effective in promoting cell growth after serum is removed from the culture medium.

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Tenascin-C affects invasiveness of EGFR-mutated lung adenocarcinoma through a putative paracrine loop
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Tenascin C (TNC) is an extracellular matrix (ECM) protein and a potential biomarker affecting progression of different tumor types, such as pancreatic and lung cancer. Alternative splicing variants of TNC are known to have an impact on interaction partners like other ECM proteins or cell surface receptors, including epidermal growth factor receptor (EGFR), leading to numerous and sometimes opposite roles of TNC in tumor cell dissemination and proliferation. Only little is known about the impact of TNC on biologic characteristics of lung cancer, such as invasion and metastatic potential. In the present study, we could link an increased expression of TNC in lung adenocarcinoma (LUAD) tissues with an unfavorable clinical outcome of patients. Furthermore, we investigated the functional role of TNC in LUAD. Immunohistochemical staining of TNC revealed a significant increase of TNC levels in primary tumours and metastases compared to normal lung tissue. Additionally, a significant correlation between TNC mRNA expression and EGFR copy number and protein expression levels has been determined. Moreover, inhibition of TNC in lung fibroblasts led to reduced invasiveness of LUAD cells harboring EGFR-activating mutations and to a shorter lamellipodia perimeter and a reduced lamellipodia area on the surface of LUAD cells. This study provides the evidence that TNC expression might be a biological relevant factor in LUAD progression in an EGFR-dependent manner and that it regulates tumor cell invasion by rearrangement of the actin cytoskeleton, especially affecting lamellipodia formation.
TNN is first linked to auditory neuropathy
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Autosomal recessive nonsyndromic auditory neuropathy is attributed to a genetic etiology. We identified a compound heterozygous missense variant, c.G736A (p.G246S) and c.C2954T (p.T985 M) in TNN of affected patients in a pedigree via candidate gene screening and exome sequencing. To determine the genetic etiology of deafness in the pedigree with a heterozygous missense variant in the gene TNN encoding tenascin-W associated with autosomal recessive nonsyndromic auditory neuropathy, the cochlear expression of tenascin-W was evaluated at mRNA and protein levels in mice, and Tnn knock out mice were generated and utilized to study the function of Tnn in the auditory system. Immunofluorescence stainings showed that tenascin-W was mainly expressed in the somatic cytoplasm of spiral ganglion neurons of mice. Homozygous Tnn knockout was lethal in mice, whereas Tnn heterozygous mice showed decreases in spiral ganglion neuron density and progressive hearing loss. We demonstrate that tenascin-W is expressed in the murine cochleae and is essential for the development of spiral ganglion neurons. An abnormal expression of tenascin-W can influence the development and function of SGNs and affect the function of the auditory system.
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Large format, subgross, three-dimensional histopathologic images of breast cancer subtypes and their corresponding imaging biomarkers were correlated with large format thin section histopathology and long-term patient outcome.
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Classification of breast cancers according to their site of origin helps overcome the inconsistencies in the current histopathologic terminology with its ductal-lobular dichotomy. The ability of the imaging biomarkers to determine the site of tumour origin and serve as a prognostic indicator emphasizes the increasingly crucial role of breast imaging in the management of breast cancer. Basing breast cancer management upon anatomically relevant terminology challenges the conventional mindset. Our proposals are based on research results from an unprecedented number of prospectively collected nonpalpable breast cancers diagnosed at their earliest detectable phases and followed up for several decades. This article is a general introduction to a series of forthcoming articles describing in detail the breast malignancies originating from the three sites of origin.
Restorative and pain-relieving effects of fibroin in preclinical models of tendinopathy
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The term tendinopathy indicates a wide spectrum of conditions characterized by alterations in tendon tissue homeostatic response and damage to the extracellular matrix. The current pharmacological approach involves the use of nonsteroidal anti-inflammatory drugs and corticosteroids often with unsatisfactory results, making essential the identification of new treatments. In this study, the pro-regenerative and protective effects of an aqueous fibroin solution (0.5–500 μg/mL) against glucose oxidase (GOx)-induced damage in rat tenocytes were investigated. Then, fibroin anti-hyperalgesic and protective actions were evaluated in two models of tendinopathy induced in rats by collagenase or carrageenan injection, respectively. In vitro, 5–10 μg/mL fibroin per se increased cell viability and reverted the morphological alterations caused by GOx (0.1 U/mL). Fibroin 10 μg/mL evoked proliferative signaling upregulating the expression of decorin, scleraxin, tenomodulin (p < 0.001), FGF-2, and tenascin-C (p < 0.01) genes. Fibroin enhanced the basal FGF-2 and MMP-9 protein concentrations and prevented their GOx-mediated decrease. Furthermore, fibroin positively modulated the production of collagen type I. In vivo, the peri-tendinous injection of fibroin (5 mg) reduced the development of spontaneous pain and hypersensitivity (p < 0.01) induced by the intra-tendinous injection of collagenase; the efficacy was comparable to that of triamcinolone. The pain-relieving action of fibroin (peri-tendinous) was confirmed in the model of tendinopathy induced by carrageenan (intra-tendinous) where this fibrous protein was also able to improve tendon matrix organization, normalizing the orientation of collagen fibers. In conclusion, the use of fibroin in tendinopathies is suggested taking advantage of its excellent mechanical properties, pain-relieving effects, and ability to promote tissue regeneration processes.
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^★: Present address: Aichi Cancer Center Research Institute, Nagoya 464, Japan.

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Cell

ArticleTenascin: an extracellular matrix protein involved in tissue interactions during fetal development and oncogenesis

Abstract

J. Theor. Biol.

Dev. Biol.

J. Biol. Chem.

J. Biol. Chem.

Meth. Enzymol.

J. Biol. Chem.

Dev. Biol.

J. Biol. Chem.

Dev. Biol.

Cell

Dev. Biol.

Cell

Differentiation

TIBS

Dev. Biol.

Nerve growth factor, laminin and fibronectin promote neurite growth in human fetal sensory ganglia cultures

J. Neurosci. Res.

Structurally distinct collagen types

Ann. Rev. Biochem.

Biologically active synthetic peptides as probes of embryonic development: a competitive peptide inhibitor of fibronectin function inhibits gastrulation in amphibian embryos and neural crest cell migration in avian embryos

J. Cell Biol.

Laminin and fibronectin in cell adhesion: enhanced adhesion of cells from regenerating liver to laminin

Fibronectin from aged fibroblasts is defective in promoting cellular adhesion

J. Cell. Physiol.

Chick myotendinous antigen. I. A monoclonal antibody as a marker for tendon and muscle morphogenesis

J. Cell Biol.

Chick myotendinous antigen. II. A novel extracellular glycoprotein complex consisting of large disulfide-linked subunits

J. Cell Biol.

Development of the molar teeth in the albino mouse

Am. J. Anat.

Induction of a basement membrane glycoprotein in embryonic kidney: possible role of laminin in morphogenesis

A six-armed oligomer isolated from cell surface fibronectin preparations

Nature

Article
Tenascin: an extracellular matrix protein involved in tissue interactions during fetal development and oncogenesis