[5][6] It is expressed in the extracellular matrix of various tissues during development, disease or injury, and in restricted neurogenic areas of the central nervous system.

[10] TN-C has been shown to be upregulated under pathological conditions caused by inflammation, infection, tumorigenesis, and at sites that are subject to unique biomechanics forces.

Expression of TN-C by radial glia precedes the onset of gliogenesis, during which time it is thought to drive the differentiation of astrocytes.

This results in a multitude of TN-C subunits differing in the number and identity of fibronectin type III domain repeats.

These myriad functions are accomplished through alternative splicing of mRNA as well as the temporal activation of signal transduction pathways and/or target genes at different stages of growth or differentiation.

TN-C clearly plays a role in cell signaling as evidenced by its ability to be induced during events such as trauma, inflammation, or cancer development.

The numerous involvements with cellular functioning and signaling make TN-C a popular protein to study in developing new therapies and detection methods.

[26] In glioblastoma cells, Tenascin-C expression provides much clinical and functional significance in terms of cancer prognosis and tumor progression.