Journal
JOURNAL OF CELL COMMUNICATION AND SIGNALING
Volume 3, Issue 3-4, Pages 287-310Publisher
SPRINGER
DOI: 10.1007/s12079-009-0075-1
Keywords
Extracellular matrix; Tenascin-C; Fibronectin; Inflammation; Cancer; Tumor; Signaling; Oncogene; Cytokine; Wound healing; Arthritis; Angiogenesis
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Funding
- Region Alsace, France
- Inserm an INCa/Inserm grant
- Arthritis Research Campaign and the Medical Research Council, UK
- hospital Hautepierre
- MRC [G0700108] Funding Source: UKRI
- Medical Research Council [G0700108] Funding Source: researchfish
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The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, tissue repair and in pathological situations such as chronic inflammation and cancer. Tenascin-C interacts with several other extracellular matrix molecules and cell-surface receptors, thus affecting tissue architecture, tissue resilience and cell responses. Tenascin-C modulates cell migration, proliferation and cellular signaling through induction of pro-inflammatory cytokines and oncogenic signaling molecules amongst other mechanisms. Given the causal role of inflammation in cancer progression, common mechanisms might be controlled by tenascin-C during both events. Drugs targeting the expression or function of tenascin-C or the tenascin-C protein itself are currently being developed and some drugs have already reached advanced clinical trials. This generates hope that increased knowledge about tenascin-C will further improve management of diseases with high tenascin-C expression such as chronic inflammation, heart failure, artheriosclerosis and cancer.
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