Calcium-sensing receptor in cancer: Good cop or bad cop?
Endocrine, ISSN: 1559-0100, Vol: 35, Issue: 3, Page: 271-284
2009
- 37Citations
- 21Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations37
- Citation Indexes37
- 37
- CrossRef28
- Captures21
- Readers21
- 21
Review Description
The extracellular calcium-sensing receptor (CaR) is a versatile 'sensor' for di- and polycationic molecules in the body. CaR plays a key role in the defense against hypercalcemia by "sensing" extracellular calcium levels in the parathyroid and kidney, the key organs maintaining systemic calcium homeostasis. Although mutation of CaR gene has so far not been associated with any malignancy, aberrant functions of CaR have implications in malignant progression. One situation is loss of CaR expression, resulting in loss of growth suppressing effects of elevated extracellular Ca by CaR, reported in parathyroid adenoma and in colon carcinoma. Another situation is activation of CaR, resulting in increased production of parathyroid hormone-related peptide (PTHrP), a primary causal factor in hypercalcemia of malignancy and a contributor to metastatic processes involving bone. CaR signaling and effects have been studied in several cancers including ovarian cancers, gastrinomas, and gliomas in addition to comparatively detailed studies in breast, prostate, and colon cancers. Studies on H-500 rat Leydig cells, a xenotransplantable model of humoral hypercalcemia of malignancy has shed much light on the mechanisms of CaR-induced cancer cell growth and survival. Pharmacological agonists and antagonists of CaR hold therapeutic promise depending on whether activation of CaR is required such as in case of colon cancer or inactivating the receptor is required as in the case of breast- and prostate tumors. © 2008 Humana Press Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=68749112871&origin=inward; http://dx.doi.org/10.1007/s12020-008-9131-5; http://www.ncbi.nlm.nih.gov/pubmed/19011996; http://link.springer.com/10.1007/s12020-008-9131-5; http://www.springerlink.com/index/10.1007/s12020-008-9131-5; http://www.springerlink.com/index/pdf/10.1007/s12020-008-9131-5; https://dx.doi.org/10.1007/s12020-008-9131-5; https://link.springer.com/article/10.1007/s12020-008-9131-5
Springer Science and Business Media LLC
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