Modulation of Tumor Cell Survival, Proliferation, and Differentiation by the Peptide Derived from Tenascin-C: Implication ofβ1-Integrin Activation
Author(s) -
Takuya Iyoda,
Fumio Fukai
Publication year - 2011
Publication title -
international journal of cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 53
eISSN - 1687-8884
pISSN - 1687-8876
DOI - 10.1155/2012/647594
Subject(s) - extracellular matrix , microbiology and biotechnology , integrin , cell growth , cell adhesion , tenascin c , tenascin , context (archaeology) , cellular differentiation , biology , cell , cancer research , fibronectin , biochemistry , paleontology , gene
Cell adhesion to extracellular matrix (ECM) participates in various biological processes, such as cell survival, proliferation, differentiation, and migration. Since these processes are essential for keeping homeostasis, aberration of these processes leads to a variety of diseases including cancer. Previously, we found that a peptide derived from tenascin- (TN-) C, termed TNIIIA2, stimulates cell adhesion to ECM through activation of β 1-integrin. It has been shown that TNIIIA2 can modulate cell proliferation and differentiation. Interestingly, TNIIIA2 could not only enhance cell proliferation but also induce apoptotic cell death, depending on cellular context. In this review, we show the function of the peptide TNIIIA2 in cell survival, proliferation, and differentiation and refer to the possibility of new strategy for tumor suppression by regulating cell adhesion status using the ECM-derived functional peptides.
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