|
|||||
|
|
Tumour-associated tenascin-C isoforms promote breast cancer cell invasion and growth by matrix metalloproteinase-dependent and independent mechanisms |
|
| Authors: | Rachael A Hancox Michael D Allen Deborah L Holliday Dylan R Edwards Caroline J Pennington David S Guttery Jacqueline A Shaw Rosemary A Walker J Howard Pringle J Louise Jones |
| Institution: | (1) Department of Cancer Studies and Molecular Medicine, Infirmary Close, University of Leicester Leicester Royal Infirmary, Robert Kilpatrick Clinical Sciences Building, Leicester, LE1 5WW, UK;(2) Centre for Tumour Biology, Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK;(3) School of Biological Sciences, University of East Anglia, University Drive, Norwich, Norfolk, NR4 7TJ, UK |
| Abstract: | IntroductionThe stromal microenvironment has a profound influence on tumour cell behaviour. In tumours, the extracellular matrix (ECM) composition differs from normal tissue and allows novel interactions to influence tumour cell function. The ECM protein tenascin-C (TNC) is frequently up-regulated in breast cancer and we have previously identified two novel isoforms – one containing exon 16 (TNC-16) and one containing exons 14 plus 16 (TNC-14/16). |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |