CSE1/CAS overexpression inhibits the tumorigenicity of HT-29 colon cancer cells.

We previously reported that CSE1/CAS (CAS) overexpression in HT-29 human colon cancer cells enhances the formation of the E-cadherin/beta-catenin complex, stimulates intercellular junction formation, and stimulates polarization of HT-29 cells. Since both E-cadherin/beta-catenin interaction and epithelial cell polarization are critically related to the tumorigenicity of carcinoma cells, we studied the role of CAS in the tumorigenicity of HT-29 colon carcinoma cells. CAS overexpression in HT-29 cells decreased the intercellular gaps and increased the compactness of cell colonies. Our results show that CAS expression inhibited migration and growth of HT-29 cancer cells. In the soft agar anchorage-independent growth assays, CAS overexpression inhibited the colony size of HT-29 cells by 74%, and inhibited colony formation number of HT-29 cells by 38%. CAS overexpression also inhibited the growth of HT-29 cells in nude mice. Our results indicate that CAS inhibits the tumorigenicity of HT-29 human colon cancer cells and, thus, it is worthwhile to further study CAS's possible role in the control of human colon cancer.