A functional variant in TNXB promoter associates with the risk of esophageal squamous‐cell carcinoma

Yang, Nan; Tian, Jianbo; Wang, Xiaoyang; Mei, Shufang; Zou, Detang; Peng, Xiaobo; Zhu, Ying; Yang, Yang; Gong, Yajie; Ke, Juntao; Zhong, Rong; Chang, Jiang

doi:10.1002/mc.23166

Cited by 8 publications

(6 citation statements)

References 37 publications

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“…On the other hand, there have been several reports of TNX expression being downregulated during tumor progression in astrocytomas (33), cutaneous melanoma (34), and neurofibromatosis type 1 (35), findings that are mostly opposite to those for TNC. Intriguingly, it has also been reported that TNX has a tumor suppressor role in cervical cancer via LINC01305 expression which modulates TNX expression (22), esophageal squamous-cell carcinoma (36), and lung cancer via LINC01305 expression (23) and that TNX is downregulated in these tumors. In agreement with the tumor suppressor role of TNX in cancer progression, TNX-deficient mice with grafted melanoma cells exhibited promotion of tumor invasion and metastasis because of increased activities of matrix metalloproteinases (MMPs) (37,38).…”

Section: Tnx Expression In Cancersmentioning

confidence: 99%

The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases

Matsumoto

Aoki

2020

Front. Immunol.

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Tenascins are a family of multifunctional extracellular matrix (ECM) glycoproteins with time- and tissue specific expression patterns during development, tissue homeostasis, and diseases. There are four family members (tenascin-C, -R, -X, -W) in vertebrates. Among them, tenascin-X (TNX) and tenascin-C (TNC) play important roles in human pathologies. TNX is expressed widely in loose connective tissues. TNX contributes to the stability and maintenance of the collagen network, and its absence causes classical-like Ehlers-Danlos syndrome (clEDS), a heritable connective tissue disorder. In contrast, TNC is specifically and transiently expressed upon pathological conditions such as inflammation, fibrosis, and cancer. There is growing evidence that TNC is involved in inflammatory processes with proinflammatory or anti-inflammatory activity in a context-dependent manner. In this review, we summarize the roles of these two tenascins, TNX and TNC, in cardiovascular and inflammatory diseases and in clEDS, and we discuss the functional consequences of the expression of these tenascins for tissue homeostasis.

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Section: Tnx Expression In Cancersmentioning

confidence: 99%

The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases

Matsumoto

Aoki

2020

Front. Immunol.

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“…In addition, silencing of long non-coding RNA (LncRNA) LINC01305 inhibited the progression of lung cancer by activating the TNX-mediated phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway ( Yan et al, 2020 ). Moreover, it has been revealed that a functional variant in the TNXB promoter is associated with risk of esophageal squamous-cell carcinoma (ESCC) in the Chinese population, leading to the expression of TNXB being downregulated in ESCC tissues ( Chang et al, 2018 ; Yang et al, 2020 ). Knockout of TNXB significantly increased cell proliferation of ESCC cells ( Yang et al, 2020 ).…”

Section: Tnx With Tumor Suppressive Functionmentioning

confidence: 99%

“…Moreover, it has been revealed that a functional variant in the TNXB promoter is associated with risk of esophageal squamous-cell carcinoma (ESCC) in the Chinese population, leading to the expression of TNXB being downregulated in ESCC tissues ( Chang et al, 2018 ; Yang et al, 2020 ). Knockout of TNXB significantly increased cell proliferation of ESCC cells ( Yang et al, 2020 ). These results suggest that TNX has a tumor suppressor role.…”

Section: Tnx With Tumor Suppressive Functionmentioning

confidence: 99%

Tenascin-X as a causal gene for classical-like Ehlers-Danlos syndrome

Okuda‐Ashitaka

Matsumoto

2023

Front. Genet.

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Tenascin-X (TNX) is an extracellular matrix glycoprotein for which a deficiency results in a recessive form of classical-like Ehlers-Danlos syndrome (clEDS), a heritable connective tissue disorder with hyperextensible skin without atrophic scarring, joint hypermobility, and easy bruising. Notably, patients with clEDS also suffer from not only chronic joint pain and chronic myalgia but also neurological abnormalities such as peripheral paresthesia and axonal polyneuropathy with high frequency. By using TNX-deficient (Tnxb−/−) mice, well-known as a model animal of clEDS, we recently showed that Tnxb−/− mice exhibit hypersensitivity to chemical stimuli and the development of mechanical allodynia due to the hypersensitization of myelinated A-fibers and activation of the spinal dorsal horn. Pain also occurs in other types of EDS. First, we review the underlying molecular mechanisms of pain in EDS, especially that in clEDS. In addition, the roles of TNX as a tumor suppressor protein in cancer progression have been reported. Recent in silico large-scale database analyses have shown that TNX is downregulated in various tumor tissues and that high expression of TNX in tumor cells has a good prognosis. We describe what is so far known about TNX as a tumor suppressor protein. Furthermore, some patients with clEDS show delayed wound healing. Tnxb−/− mice also exhibit impairment of epithelial wound healing in corneas. TNX is also involved in liver fibrosis. We address the molecular mechanism for the induction of COL1A1 by the expression of both a peptide derived from the fibrinogen-related domain of TNX and integrin α11.

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“…Further analysis revealed that the risk score was independent of other clinical information in the ESCA prognosis model. TNXB knockout has been shown to promote the proliferation of esophageal carcinoma cells, suggesting that TNXB plays a tumor-suppressive role by inhibiting the proliferation of esophageal carcinoma cells [43]. STK31 has been implicated in promoting the progression of pancreatic cancer by enhancing cell proliferation, migration, and invasion.…”

Section: Rt-qpcr Validation For the Expression Of Pla2g2f Hhip Tnxb A...mentioning

confidence: 99%

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

Huang,

Wang,

Lin

et al. 2023

Preprint

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Background Esophageal cancer (ESCA) is a prevalent form of cancer with a grim prognosis. It has been reported that 5-methylcytosine (m5C) regulators are closely linked to carcinogenesis and distant metastasis. However, the role of m5C regulator in ESCA is still elusive. The aim of this study was to investigate the connections between m5C regulators and the initiation and progression of ESCA, with a particular focus on prognosis. Methods Gene expression profile data from TCGA database, including 11 normal and 142 tumor tissues, were obtained and divided into two ESCA subtypes according to the m5C regulators expression. Differentially expressed genes (DEGs) of two ESCA subtypes, normal and tumor tissues from TCGA, and normal and tumor tissues from validation datasets were analyzed. Inter-DEGs were filtered from the overlap of three sets of DEGs which named inter-DEGs. Functional analysis, immune infiltration analysis, drug sensitivity analysis, prognosis model was carried out to investigate the biological function and potential role of m5C regulators in ESCA. The expression of PLA2G2F, HHIP, TNXB, and STK31 in ESCA and adjacent esophageal tissues was detected by RT-qPCR. Results The expression of m5C regulators, namely TRDMT1, NSUN2, NSUN4, NSUN6, DNMT1, ALYREF, and YBX1, were upregulated in ESCA subtype 2 group. Correlation analysis demonstrated that m5C regulators positively correlated with E2F targets, G2M checkpoint, MYC targets V1, while negatively correlated with TNF-α signaling via NF-kB, and Notch signaling pathway. Additionally, the immune infiltration analysis indicated that m5C regulators was positively correlated with Macrophages M0, and negatively correlated with T cells CD8 infiltration. 4 independent prognostic genes, including PLA2G2F, HHIP, TNXB, and STK31, were selected to construct prognostic model and exhibited good function in predicting the prognosis of ESCA patients. RT-qPCR was used to validate the gene expression that the PLA2G2 had higher expression in ESCA tissues compared to adjacent tissues, while the expression of STK31, HHIP, and TNXB showed down regulation in ESCA tissues. Conclusions This study explored the comprehensive feature of 2 subtypes of m5C regulators in ESCA patients, which may improve understanding of m5C regulation in the tumor biology of ESCA.

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A functional variant in TNXB promoter associates with the risk of esophageal squamous‐cell carcinoma

Cited by 8 publications

References 37 publications

The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases

The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases

Tenascin-X as a causal gene for classical-like Ehlers-Danlos syndrome

Identification and Validation of a Prognostic Signature of m 5 C-Related Genes for Esophageal Cancer

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