posted on 2012-10-24, 09:00authored byR. A. Alcock, J. H. Pringle, J. A. Shaw, D. L. Holliday, M. Allen, R. A. Walker, J. L. Jones
Background:
Cellular interactions with the extracellular matrix (ECM) control many aspects of cell function. The complex ECM protein Tenascin-C (TN), which exists as multiple isoforms, is upregulated in breast cancer. We previously have identified a change in the TN isoform profile in breast cancer, with detection of two additional isoforms — TN16 and TN14/16 — not seen in normal breast [1]. The purpose of this study was to investigate directly the effects of these tumour-associated TNC isoforms on breast cancer cell behaviour.