Uncontrolled proliferation and invasion are the two defining hallmarks of cancer. Invasion and subsequent metastasis offer the greatest challenge for the clinical management and treatment of cancer. By the time of diagnosis, many cancers have invaded locally and already metastasised to distant sites, where the cells can remain dormant only to become activated at a later date and cause renewed problems following therapy. It is therefore important to target the invasive component of cancer through the identification of genes that control and mediate invasion and subsequent metastasis.

Our research focuses on the contribution AP-1 makes to tumorigenesis by identifying AP-1 target genes that mediate invasion. Recently, we have established tractable human models to identify AP-1-dependent differentially-expressed genes to define further the invasion programme. We have used gene expression profiling to identify AP-1 target genes in transformed rat and human fibroblasts, and in human squamous cell carcinoma derived cell lines. Functional analysis of differentially expressed genes demonstrates that up-regulated genes function as effectors of invasion, whilst down-regulated genes function as suppressors of invasion.

The long-term aim is to validate constituent genes involved in the invasion programme as targets for the sdevelopment of diagnostics and therapeutics for human tumours.