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

Semin Oncol. 1999 Apr;26(2):227-33.


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-CAM1, a cell-adhesion molecule (CAM) isoform (I), was recently shown to play a critical role in prostate cancer initiation and progression. Loss of C-CAM1 expression occurs early in the development of prostate cancer, suggesting that C-CAM1 may help maintain the differentiated state of the prostate epithelium. Reintroduction of C-CAM1 into cancer cells can reverse their cancerous growth. Thus, the C-CAM1 molecule itself or drugs that increase C-CAM1 expression are promising agents for prostate cancer treatment. The mechanisms by which C-CAM1 suppresses tumorigenesis are different from those of p53 and Rb. Therefore, C-CAM1 therapy is a new form of prostate cancer treatment. To exploit C-CAM1's therapeutic potential, a human C-CAM1 adenovirus expression vector (Ad-hu-C-CAM1) 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-CAM1-mediated tumor suppression may also help us design better strategies for prevention and treatment for prostate cancer.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adenosine Triphosphatases / genetics
  • Adenosine Triphosphatases / physiology
  • Adenosine Triphosphatases / therapeutic use*
  • Animals
  • Antigens, CD
  • Carcinoembryonic Antigen
  • Cell Adhesion
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / physiology
  • Cell Adhesion Molecules / therapeutic use*
  • Cell Differentiation
  • Epithelial Cells / physiology
  • Gene Expression Regulation, Neoplastic
  • Genes, Retinoblastoma / genetics
  • Genes, Tumor Suppressor / genetics
  • Genes, p53 / genetics
  • Genetic Therapy
  • Genetic Vectors
  • Glycoproteins
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Neoplasm Transplantation
  • Oncogenes / genetics
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / physiopathology
  • Prostatic Neoplasms / prevention & control


  • Antigens, CD
  • CD66 antigens
  • Carcinoembryonic Antigen
  • Ceacam1 protein, mouse
  • Ceacam2 protein, mouse
  • Cell Adhesion Molecules
  • Glycoproteins
  • Adenosine Triphosphatases