Navneet SinghMoltira PromkanGuangming LiuJames VaraniSubhas ChakrabartySouthern Illinois University School of MedicineMahidol UniversityUniversity of Michigan Medical School2018-10-192018-10-192013-01-01Best Practice and Research: Clinical Endocrinology and Metabolism. Vol.27, No.3 (2013), 455-463153219081521690X2-s2.0-85027945625https://repository.li.mahidol.ac.th/handle/20.500.14594/31417The extracellular Ca2+-sensing receptor (CaSR) is a robust promoter of differentiation in colonic epithelial cells and functions as a tumor suppressor in colon cancer. CaSR mediates its biologic effects through diverse mechanisms. Loss of CaSR expression activates a myriad of stem cell-like molecular features that drive and sustain the malignant and drug-resistant phenotypes of colon cancer. This CaSR-null phenotype, however, is not irreversible and induction of CaSR expression in CaSR-null cells promotes cell death mechanisms and restores drug sensitivity. The CaSR also functions as a tumor suppressor in breast cancer and promotes cellular sensitivity to cytotoxic drugs. BRCA1 and CaSR functions intersect in breast cancer cells, and CaSR activation can rescue breast cancer cells from the deleterious effect of BRCA1 mutations. © 2013 Elsevier Ltd. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineConference PaperSCOPUS10.1016/j.beem.2013.04.001