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- W2182169145 abstract "Background The classical role of the calcium-sensing receptor (CaSR), an extracellular G protein-coupled receptor, is regulation of calcium homeostasis. In addition, it is involved in several cellular processes such as proliferation, differentiation, and apoptosis. The CaSR has been suggested to mediate the effects of calcium in delaying the onset of colorectal cancer (CRC). We have previously demonstrated that CaSR expression is downregulated in CRC, leading us to hypothesize that loss of CaSR might provide a growth advantage to transformed cells, conferring them resistance to calciummediated growth inhibition. Therefore the aim of the study was to understand the consequences of losing CaSR expression in CRC. Methods and Results We analysed mRNA (qRT-PCR) and protein (immunofluorescence) expression of CaSR in two CRC cell lines: Caco-2/15 (well-differentiated adenocarcinoma) and HT-29 (moderately differentiated adenocarcinoma). HT-29 cells showed lower CaSR levels when compared with Caco-2/15 cells (30-fold lower mRNA expression), similar to our CRC patient cohort (n = 60), where we found significantly less CaSR expression in tumours compared with respective adjacent mucosa (p < 0.001). To investigate the possible impact of CaSR on growth, we used a" @default.
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- W2182169145 date "2013-01-01" @default.
- W2182169145 modified "2023-10-17" @default.
- W2182169145 title "Loss of the Calcium-Sensing Receptor Provides a Growth Advantage to Colon Cancer Cells" @default.
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