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Background Each year breast cancer is diagnosed in approximately 1 million women worldwide [1]. Our lab has previously linked Junctional Adhesion Molecule A (JAM-A) gene and protein over-expression in breast tumours with an increased risk of metastasis [2,3]. JAM-A loss or inhibition has also been shown to inhibit cell migration and invasion [2], while increasing apoptosis possibly as a result of increased HER2 degradation and downstream Akt signalling [3]. A novel JAM-A inhibitor was designed by our lab which has been found to reduce the migration and proliferation of 4T1 breast cancer cells in vitro, and reduce 4T1 tumour growth in vivo. In this study we sought to determine both the stability and the efficacy of the JAM-A inhibitor on cell proliferation and cell signalling.

Functions of novel Junctional Adhesion Molecule-A (JAM-A) inhibitor in breast cancer cells