In 1994 we first described CD97, a member of the EGF-TM7 subfamily of adhesion-GPCRs. During the next few years we showed that, in contrast to the other EGF-TM7 molecules, CD97 is broadly distributed and not restricted to the hematopoetic system. Normal and malignant cells of epithelial and mesechymal origin are CD97 positive.
The main focus of our work is to characterize the function of CD97 outside the immune system. Transgenic mice, selectively overexpressing CD97 in enterocytes, were the key to find out an unexpected role of CD97: it strengthens basolateral cell contacts of normal epithelia cells. However, during colorectal carcinogenesis CD97 is translocated into the cytoplasm. This process implies a dramatic change of function of CD97: it increases single random tumor cell migration.
Our current studies are related to the association and the interplay of membrane-bound and cytoplasmic CD97 with signal transduction pathways. The fact that CD97 truncation at the seven-span transmembrane domains impedes the function of CD97 in vivo and in vitro, suggests signal transduction of CD97 through its beta-chain without ligand binding.