Function and therapeutic implication of C-CAM cell-adhesion molecule in prostate cancer

Human neoplasms are often caused by cumulative alterations in oncogenes and tumor-suppressor genes. By identifying the early genetic changes involved in tumorigenesis, one can develop strategies to prevent and detect cancers at early stages, when treatment is most effective. C-CAMI, a cell-adhesion molecule (CAM) isoform (I), was recently shown to play a critical role in prostate cancer initiation and progression. Loss of C-CAMI expression occurs early in the development of prostate cancer, suggesting that C-CAMI may help maintain the differentiated state of the prostate epithelium. Reintroduction of C-CAMI into cancer cells can reverse their cancerous growth. Thus, the C- CAMI molecule itself or drugs that increase C-CAMI expression are promising agents for prostate cancer treatment. The mechanisms by which C-CAMI suppresses tumorigenesis are different from those of p53 and Rb. Therefore, C-CAMI therapy is a new form of prostate cancer treatment. To exploit C- CAMI's therapeutic potential, a human C-CAMI adenovirus expression vector (Ad-hu-C-CAM) has been used to treat prostate tumor xenografts in nude mice. The preliminary results have shown great promise. In addition, while C-CAM gene therapy may have immediate application in prostate cancer treatment, the knowledge to be learned from mechanistic studies of C-CAMI-mediated tumor suppression may also help us design better strategies for prevention and treatment for prostate cancer.