We have previously shown that COX-2 mediated VEGF-C upregulation in human breast cancer cell lines [7], [9] confers a prometastatic phenotype by two mechanisms: increased ability for inducing lymphangiogenesis in situ [9] and an autocrine stimulation of motility by utilizing a diverse family of VEGF-C receptors [8]. Here, MT-CO2 is linked to breast carcinoma.