Tenascin-X: beyond the architectural function

Valcourt, Ulrich; Alcaraz, Lindsay B.; Exposito, Jean‐Yves; Lethias, Claire; Bartholin, Laurent

doi:10.4161/19336918.2014.994893

Cited by 99 publications

(87 citation statements)

References 87 publications

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“…8 Tenascin-X is primarily involved in the process of organogenesis by supporting cell migration, while the expression of TNXB is higher in malignant mesothelioma (MM) when compared with that of ovarian/peritoneal serous carcinoma. 36,37 Matrix metal- of that kinase. 40,41 Reports have correlated down-regulated E-cadherin and up-regulated vimentin with enhanced migration of tumour cells, leading to higher metastatic risk of patients with head and neck squamous cell carcinomas.…”

Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

Yan

Chu

Qiu

et al. 2019

J Cellular Molecular Medi

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Cervical cancer (CC) remains one of the leading malignancies afflicting females worldwide, with its aetiology associated with long‐term papillomavirus infection. Recent studies have shifted their focus and research attention to the relationship between long non‐coding RNAs (lncRNAs) and CC therapeutic. Thus, the aim of the current study was to investigate the underlying mechanism of lncRNA LINC01305 on the cell invasion, migration and epithelial‐mesenchymal transition (EMT) of CC cells via modulation of the PI3K/Akt signalling pathway by targeting tenascin‐X B (TNXB). The expressions of LINC01305, TNXB, MMP2, MMP9, E‐cadherin, vimentin, PI3K, Akt, p‐PI3K, p‐Akt and TNXB were detected in this study. After which, the cell invasion and migration abilities of the CC cells were determined respectively. Bioinformatics and the application of a dual luciferase reporter gene assay provided verification indicating that TNXB is the target gene of lncRNA LINC01305. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis methods revealed that the expressions of MMP2, MMP9, vimentin, PI3K, Akt, p‐PI3K and p‐Akt were decreased following the down‐regulation of LncRNA LINC01305 or overexpression of TNXB. LncRNA LINC01305 silencing or TNXB overexpression was noted to decrease the migration and invasion of SiHa cells. Taken together, the key findings of the current study present evidence suggesting that lncRNA LINC01305 silencing suppresses EMT, invasion and migration via repressing the PI3K/Akt signalling pathway by means of targeting TNXB in CC cells, which ultimately provides novel insight and identification of potential therapeutic targets for CC.

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Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

Yan

Chu

Qiu

et al. 2019

J Cellular Molecular Medi

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“…Tenascin-X (TNX) is an extracellular matrix glycoprotein belonging to a family of tenascins and other molecules that governs tissue structure (Valcourt et al 2015). Its absence leads to heritable connective tissue disorders with a phenotype similar to hypermobility Ehlers-Danlos Syndrome (hEDS) (Zweers et al 2004), although TNX deficient patients are now classified as a separate subgroup (Malfait et al 2017).…”

Section: Introductionmentioning

confidence: 99%

A novel role for the extracellular matrix glycoprotein‐Tenascin‐X in gastric function

Aktar

Peiris

Fikree

et al. 2019

The Journal of Physiology

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Key points Tenascin X (TNX) functions in the extracellular matrix of skin and joints where it maintains correct intercellular connections and tissue architecture TNX is associated exclusively with vagal‐afferent endings and some myenteric neurones in mouse and human stomach, respectively. TNX‐deficient mice have accelerated gastric emptying and hypersensitivity of gastric vagal mechanoreceptors that can be normalized by an inhibitor of vagal‐afferent sensitivity. Cultured nodose ganglion neurones showed no changes in response to capsaicin, cholecystokinin and potassium chloride in TNX‐deficient mice. TNX‐deficient patients have upper gastric dysfunction consistent with those in a mouse model. Our translational studies suggest that abnormal gastric sensory function may explain the upper gut symptoms present in TNX deficient patients, thus making it important to study gastric physiology. TNX deficiency should be evaluated routinely in patients with connective tissue abnormalities, which will enable a better understanding of its role and allow targeted treatment. For example, inhibitors of vagal afferents‐baclofen could be beneficial in patients. These hypotheses need confirmation via targeted clinical trials. Abstract Tenascin‐X (TNX) is a glycoprotein that regulates tissue structure via anti‐adhesive interactions with collagen in the extracellular matrix. TNX deficiency causes a phenotype similar to hypermobility Ehlers–Danlos syndrome involving joint hypermobility, skin hyperelasticity, pain and gastrointestinal dysfunction. Previously, we have shown that TNX is required for neural control of the bowel by a specific subtype of mainly cholinergic enteric neurones and regulates sprouting and sensitivity of nociceptive sensory endings in mouse colon. These findings correlate with symptoms shown by TNX‐deficient patients and mice. We aimed to identify whether TNX is similarly present in neural structures found in mouse and human gastric tissue. We then determined whether TNX has a functional role, specifically in gastric motor and sensory function and nodose ganglia neurones. We report that TNX was present in calretinin‐immunoreactive extrinsic nerve endings in mouse and human stomach. TNX deficient mice had accelerated gastric emptying and markedly increased vagal afferent responses to gastric distension that could be rescued with GABA B receptor agonist. There were no changes in nodose ganglia excitability in TNX deficient mice, suggesting that vagal afferent responses are probably the result of altered peripheral mechanosensitivity. In TNXB‐deficient patients, significantly greater symptoms of reflux, indigestion and abdominal pain were reported. In the present study, we report the first role for TNX in gastric function. Further studies are required in TNX deficient patients to determine whether symptoms can be relieved usin...

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“…It was recently reported that Tnx also modulates the effects of growth factors. For example, TNX reportedly activates the latent form of endogenous TGFb1 and accelerates epithelialmesenchymal transition in cell culture [35,36]. Furthermore, we reported that TNX binds to both VEGF-A and -B and facilitates VEGF-B/VEGF-R1 receptor-mediated proliferation of vascular endothelial cells [37,38].…”

Section: Introductionmentioning

confidence: 99%

Loss of tenascin X gene function impairs injury‐induced stromal angiogenesis in mouse corneas

Sumioka

Iwanishi

Okada

et al. 2017

J Cellular Molecular Medi

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To determine the contribution by tenascin X (Tnx) gene expression to corneal stromal angiogenesis, the effects were determined of its loss on this response in TNX knockout (KO) mice. In parallel, the effects of such a loss were evaluated on vascular endothelial growth factor (VEGF) and transforming growth factor b1 (TGFb1) gene and protein expression in fibroblasts and macrophages in cell culture. Histological, immunohistochemical and quantitative RT-PCR changes determined if Tnx gene ablation on angiogenic gene expression, inflammatory cell infiltration and neovascularization induced by central corneal stromal cauterization. The role was determined of Tnx function in controlling VEGF-A or TGFb1 gene expression by comparing their expression levels in ocular fibroblasts and macrophages obtained from wild-type (WT) and bodywide Tnx KO mice. Tnx was up-regulated in cauterized cornea. In Tnx KO, macrophage invasion was attenuated, VEGF-A and its cognate receptor mRNA expression along with neovascularization were lessened in Tnx KOs relative to the changes occurring in their WT counterpart. Loss of Tnx instead up-regulated in vivo mRNA expression of anti-angiogenic VEGF-B but not VEGF-A. On the other hand, TGFb1 mRNA expression declined in Tnx KO cultured ocular fibroblasts. Loss of Tnx gene expression caused VEGF-A expression to decline in macrophages. Tnx gene expression contributes to promoting TGFb1 mRNA expression in ocular fibroblasts and VEGF-A in macrophages, macrophage invasion, up-regulation of VEGF-A expression and neovascularization in an injured corneal stroma. On the other hand, it suppresses anti-angiogenic VEGF-B mRNA expression in vivo.

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Tenascin-X: beyond the architectural function

Cited by 99 publications

References 87 publications

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

Retracted: LncRNA LINC01305 silencing inhibits cell epithelial‐mesenchymal transition in cervical cancer by inhibiting TNXB‐mediated PI3K/Akt signalling pathway

A novel role for the extracellular matrix glycoprotein‐Tenascin‐X in gastric function

Loss of tenascin X gene function impairs injury‐induced stromal angiogenesis in mouse corneas

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