Published online Sep 15, 2021. doi: 10.4251/wjgo.v13.i9.980
Peer-review started: February 21, 2021
First decision: May 8, 2021
Revised: June 3, 2021
Accepted: August 11, 2021
Article in press: August 11, 2021
Published online: September 15, 2021
Processing time: 201 Days and 3.2 Hours
Tenascin-C (TNC) is an adhesion modulatory protein present in the extracellular matrix that is highly expressed in several malignancies, including colon cancer. Although TNC is considered a negative prognostic factor for cancer patients, the substantial role of the TNC molecule in colorectal carcinogenesis and its malignant progression is poorly understood. We previously found that TNC has a cryptic functional site and that a TNC peptide containing this site, termed TNIIIA2, can potently and persistently activate beta1-integrins. In contrast, the peptide FNIII14, which contains a cryptic bioactive site within the fibronectin molecule, can inactivate beta1-integrins. This review presents the role of TNC in the development of colitis-associated colorectal cancer and in the malignant progression of colon cancer, particularly the major involvement of its cryptic functional site TNIIIA2. We propose new possible prophylactic and therapeutic strategies based on inhibition of the TNIIIA2-induced beta1-integrin activation by peptide FNIII14.
Core Tip: Exposure of the cryptic functional site TNIIIA2 from the Tenascin-C (TNC) molecule and its potent and sustained activation of beta1-integrins appear to be associated with the development of colon cancer and its malignant progression. Inhibition of the biological function of TNIIIA2 derived from TNC molecule may be a promising strategy for the prevention and treatment of colon cancer.