Roles for the calcium sensing receptor in primary and metastatic cancer

A. T. Manning, N. O'Brien, M. J. Kerin

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18 Citations (Scopus)

Abstract

Aim: To review the role of the calcium sensing receptor (CASR) in colorectal, breast and parathyroid cancers and related cell lines, and to discuss the effects of CASR in the setting of bone metastases from breast cancer. Methods: We performed a literature search of the PubMed database of the National Library of Medicine (NLM) to identify articles concerning the CASR's involvement in different cancers. Further relevant papers were obtained from the references of those identified in the original search. Results: Loss of CASR expression is understood to be associated with abnormal differentiation and progression of colorectal carcinoma. It is expressed in both normal and malignant breast tissues and has been implicated in the vicious cycle of bone metastases through its interactions with the parathyroid hormone related peptide (PTHrP). In parathyroid tissue, CASR expression has been linked to proliferation of both parathyroid adenomas and carcinomas. Conclusion: Apart from its role in calcium homeostasis, the CASR has many diverse functions in a variety of tissue types throughout the body, and is involved in various signalling pathways relating to cell proliferation and differentiation. CASR has been shown to be involved in the progression and spread of a variety of cancers such as colorectal, breast and parathyroid, and is likely to be the focus of much research to further elucidate its precise role.

Original languageEnglish
Pages (from-to)693-697
Number of pages5
JournalEuropean Journal of Surgical Oncology
Volume32
Issue number7
DOIs
Publication statusPublished - 1 Sep 2006

Keywords

  • Bone metastases
  • Breast cancer
  • Calcium sensing receptor (CASR)
  • Colorectal cancer
  • Parathyroid cancer
  • Parathyroid hormone-related peptide (PTHrP)

Authors (Note for portal: view the doc link for the full list of authors)

  • Authors
  • Manning, AT;O'Brien, N;Kerin, MJ

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