Src-mediated regulation of homotypic cell adhesion: implications for cancer progression and opportunities for therapeutic intervention

Abstract

Homotypic cell adhesion is fundamental to the maintenance of cell and tissue structure and function and is predominantly mediated by cadherin-containing adherens junction complexes. The integrity of these adhesion sites can be modulated by Src, a non-receptor tyrosine kinase implicated in the development and progression of a number of tumour types. Changes in homotypic cell adhesion have been shown to be central to cell migration and invasion, characteristics central to tumour metastasis and irrevocably leading to patient death. Targeting of Src may thus be an effective means to suppress migration and invasion of cancer cells and suggests the use of Src inhibitors clinically as a mechanism to delay or limit tumour spread. In this article, we review the role of Src in cell-cell adhesion and discuss data that suggests its usefulness as a therapeutic target in anti-invasive therapy.