These findings support a role for the endogenous miR-29b and/or miR-200c in the regulation of ADAM12-L gene expression at the post-transcriptional level via targeting of the unique 3′UTRs of ADAM12-L. Since the translation product of ADAM12-L differs from the protein product of ADAM12-S in its biochemical properties, cellular localization, and most likely substrate specificity and function, better understanding of the mechanisms controlling expression of each splice variant is an important step in the research on ADAM12 in breast cancer. Here, ADAM12 is linked to breast cancer.