Tenascin-C protein is induced by Transforming Growth Factor-ß1 but does not correlate with time to tumor progression in high-grade gliomas

2005 ◽  
Vol 77 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Peter Hau ◽  
Leoni A. Kunz-Schughart ◽  
Petra Rümmele ◽  
Füsun Arslan ◽  
Anett Dörfelt ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Progression ◽  
Transforming Growth Factor ◽  
High Grade ◽  
C Protein ◽  
Tenascin C ◽  
Transforming Growth Factor ß1 ◽  
High Grade Gliomas ◽  
Time To Tumor Progression

scholarly journals Inflammation and tumor progression: signaling pathways and targeted intervention

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Huakan Zhao ◽  
Lei Wu ◽  
Guifang Yan ◽  
Yu Chen ◽  
Mingyue Zhou ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Progression ◽  
Signaling Pathways ◽  
Transforming Growth Factor ◽  
Response To Therapy ◽  
Janus Kinase ◽  
Oncolytic Viruses ◽  
Mitogen Activated Protein Kinase ◽  
Resolution Of Inflammation ◽  
Chemokine Ligands

AbstractCancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates tumor progression and treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells (DCs) and antigen presentation, leading to anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers and activators of transcription (JAK-STAT), toll-like receptor (TLR) pathways, cGAS/STING, and mitogen-activated protein kinase (MAPK); inflammatory factors, including cytokines (e.g., interleukin (IL), interferon (IFN), and tumor necrosis factor (TNF)-α), chemokines (e.g., C-C motif chemokine ligands (CCLs) and C-X-C motif chemokine ligands (CXCLs)), growth factors (e.g., vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β), and inflammasome; as well as inflammatory metabolites including prostaglandins, leukotrienes, thromboxane, and specialized proresolving mediators (SPM), have been identified as pivotal regulators of the initiation and resolution of inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, and SPM have been developed to specifically modulate inflammation in cancer therapy, with some of these factors already undergoing clinical trials. Herein, we discuss the initiation and resolution of inflammation, the crosstalk between tumor development and inflammatory processes. We also highlight potential targets for harnessing inflammation in the treatment of cancer.

Transforming growth factor beta 1 dependent regulation of Tenascin-C in radiation impaired wound healing

2004 ◽  
Vol 72 (3) ◽  
pp. 297-303 ◽  
Author(s):  
Falk Wehrhan ◽  
Franz Rödel ◽  
Gerhard G. Grabenbauer ◽  
Kerstin Amann ◽  
Wolfgang Brückl ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Impaired Wound Healing ◽  
Tenascin C ◽  
Growth Factor Beta

Regulation of mesenchymal extracellular matrix protein synthesis by transforming growth factor-beta and glucocorticoids in tumor stroma

1995 ◽  
Vol 108 (6) ◽  
pp. 2153-2162 ◽  
Author(s):  
J.F. Talts ◽  
A. Weller ◽  
R. Timpl ◽  
M. Ekblom ◽  
P. Ekblom
Keyword(s):  
Extracellular Matrix ◽  
Growth Factors ◽  
Growth Factor ◽  
Mrna Expression ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tenascin C ◽  
Extracellular Matrix Components ◽  
Growth Factor Beta ◽  
Matrix Components

We have here studied the composition and regulation of stromal extracellular matrix components in an experimental tumor model. Nude mice were inoculated with WCCS-1 cells, a human Wilms' tumor cell line. In the formed tumors the stroma was found to contain mesenchymal extracellular matrix proteins such as tenascin-C, fibulins-1 and 2 and fibronectin, but no nidogen. Nidogen was confined to basement membranes of tumor blood vessels. Since glucocorticoids have been shown to downregulate tenascin-C expression in vitro, we tested whether dexamethasone can influence biosynthesis of extracellular matrix components during tumor formation in vivo. A downregulation of tenascin-C mRNA and an upregulation of fibronectin mRNA expression by dexamethasone was noted. Transforming growth factor-beta 1 mRNA levels were unaffected by the dexamethasone treatment. Glucocorticoids can thus downregulate tenascin-C synthesis although local stimulatory growth factors are present. The competition between a negative and a positive extrinsic factor on synthesis of stromal extracellular matrix components was studied in a fibroblast/preadipocyte cell line. Transforming growth factor-beta 1 stimulated tenascin-C synthesis but did not affect fibronectin or fibulin-2 synthesis. Dexamethasone at high concentrations could completely suppress the effect of transforming growth factor-beta 1 on tenascin-C mRNA expression. Transforming growth factor-beta 1 could in turn overcome the downregulation of tenascin-C mRNA expression caused by a lower concentration of dexamethasone. We therefore suggest that the limited expression of tenascin-C in part is due to a continuous suppression by physiological levels of glucocorticoids, which can be overcome by local stimulatory growth factors when present in sufficient amounts.

scholarly journals Regulation of TEAD Transcription Factors in Cancer Biology

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 600 ◽  
Author(s):  
Hyunbin Huh ◽  
Dong Kim ◽  
Han-Sol Jeong ◽  
Hyun Park
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Tumor Progression ◽  
Transforming Growth Factor Beta ◽  
Cancer Biology ◽  
Molecular Mechanisms ◽  
Cancer Metabolism ◽  
Transforming Growth Factor ◽  
Clinicopathological Parameters ◽  
Transcriptional Output

Transcriptional enhanced associate domain (TEAD) transcription factors play important roles during development, cell proliferation, regeneration, and tissue homeostasis. TEAD integrates with and coordinates various signal transduction pathways including Hippo, Wnt, transforming growth factor beta (TGFβ), and epidermal growth factor receptor (EGFR) pathways. TEAD deregulation affects well-established cancer genes such as KRAS, BRAF, LKB1, NF2, and MYC, and its transcriptional output plays an important role in tumor progression, metastasis, cancer metabolism, immunity, and drug resistance. To date, TEADs have been recognized to be key transcription factors of the Hippo pathway. Therefore, most studies are focused on the Hippo kinases and YAP/TAZ, whereas the Hippo-dependent and Hippo-independent regulators and regulations governing TEAD only emerged recently. Deregulation of the TEAD transcriptional output plays important roles in tumor progression and serves as a prognostic biomarker due to high correlation with clinicopathological parameters in human malignancies. In addition, discovering the molecular mechanisms of TEAD, such as post-translational modifications and nucleocytoplasmic shuttling, represents an important means of modulating TEAD transcriptional activity. Collectively, this review highlights the role of TEAD in multistep-tumorigenesis by interacting with upstream oncogenic signaling pathways and controlling downstream target genes, which provides unprecedented insight and rationale into developing TEAD-targeted anticancer therapeutics.

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