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Endocrinology |
Department of Molecular Pathology, University of Texas, M.D. Anderson Cancer Center, Houston, Texas 77030 [S. C., V. R.], and Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109 [H. A., J. V.]
Ca2+ has chemopreventive activity against colon cancer, albeit its mechanisms of action are not understood. In this study, we showed that four different human colon carcinoma cell lines (FET, SW480, MOSER, and CBS) expressed the human parathyroid calcium sensing receptor (CaSR) and that a function of extracellular Ca2+ and the CaSR in these cells was the promotion of E-cadherin expression and suppression of ß-catenin/T cell factor activation. We also found that human colonic crypt epithelial cells expressed the CaSR, and histologically differentiated carcinomas (i.e., where three-dimensional, crypt-like structures were present) expressed less receptor by comparison, whereas an almost complete loss of CaSR expression was observed in undifferentiated tumors. These results suggest that extracellular Ca2+ and the CaSR may function to regulate the differentiation of colonic epithelial cells and that disruption of this ligand receptor system may contribute to abnormal differentiation and malignant progression. In addition, the promotion of E-cadherin and suppression of ß-catenin/T cell factor may be an important mechanism underlying the chemopreventive action of Ca2+ in colon cancer.
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