Calcium and CaSR/IP3R in prostate cancer development
Abstract Prostate cancer (PrCa) progression and mortality are associated with calcium metabolism, parathyroid hormone level, and vitamin D level. However, the lack of comprehensive understanding on the molecular rationale of calcium intake, serum homeostasis, and cytoplasmic function, is critically...
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Format: | Article |
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BMC
2018-02-01
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Series: | Cell & Bioscience |
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Online Access: | http://link.springer.com/article/10.1186/s13578-018-0217-3 |
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author | Liyang Wang MengMeng Xu Zhongguang Li Mengting Shi Xin Zhou Xinnong Jiang Joseph Bryant Steven Balk Jianjie Ma William Isaacs Xuehong Xu |
author_facet | Liyang Wang MengMeng Xu Zhongguang Li Mengting Shi Xin Zhou Xinnong Jiang Joseph Bryant Steven Balk Jianjie Ma William Isaacs Xuehong Xu |
author_sort | Liyang Wang |
collection | DOAJ |
description | Abstract Prostate cancer (PrCa) progression and mortality are associated with calcium metabolism, parathyroid hormone level, and vitamin D level. However, the lack of comprehensive understanding on the molecular rationale of calcium intake, serum homeostasis, and cytoplasmic function, is critically hindering our ability to propose a mechanism based technique for targeting calcium in PrCa. Recently, studies performed on PrCa samples have shown that calcium-sensing receptor regulates cytoplasmic calcium levels in relation to extracellular calcium concentrations. Recent publications have also revealed the role of BAP1 and FBXL2 associated endoplasmic reticular IP3Rs in controlling the trafficking of calcium from cytosol into the mitochondria of PrCa cells. Competitive binding between BAP1, PTEN and FBXL2 to IP3Rs regulates the calcium flux of mitochondria and thereby controls apoptosis. Analysis of data released by Prostate Adenocarcinoma (Provisional TCGA) reveals that calcium related proteins play critical role in the development of PrCa. From this constantly expanding appreciation for the role of calcium outside the muscle, we predict that calcium-induced-calcium-release ryanodine receptors could also be involved in determining cell fate. |
first_indexed | 2024-12-20T06:49:46Z |
format | Article |
id | doaj.art-c52901e7dfde4a8d9bd78794218257f8 |
institution | Directory Open Access Journal |
issn | 2045-3701 |
language | English |
last_indexed | 2024-12-20T06:49:46Z |
publishDate | 2018-02-01 |
publisher | BMC |
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series | Cell & Bioscience |
spelling | doaj.art-c52901e7dfde4a8d9bd78794218257f82022-12-21T19:49:36ZengBMCCell & Bioscience2045-37012018-02-01811710.1186/s13578-018-0217-3Calcium and CaSR/IP3R in prostate cancer developmentLiyang Wang0MengMeng Xu1Zhongguang Li2Mengting Shi3Xin Zhou4Xinnong Jiang5Joseph Bryant6Steven Balk7Jianjie Ma8William Isaacs9Xuehong Xu10National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China/CGDB, Shaanxi Normal University College of Life SciencesDepartment of Pharmacology, Duke University Medical CenterNational Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China/CGDB, Shaanxi Normal University College of Life SciencesNational Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China/CGDB, Shaanxi Normal University College of Life SciencesNational Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China/CGDB, Shaanxi Normal University College of Life SciencesCollege of Life Science and Technology, Huazhong University of Science and TechnologyInstitute of Human Virology, University of Maryland School of MedicineHematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical SchoolOhio State University School of MedicineJohns Hopkins School of MedicineNational Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China/CGDB, Shaanxi Normal University College of Life SciencesAbstract Prostate cancer (PrCa) progression and mortality are associated with calcium metabolism, parathyroid hormone level, and vitamin D level. However, the lack of comprehensive understanding on the molecular rationale of calcium intake, serum homeostasis, and cytoplasmic function, is critically hindering our ability to propose a mechanism based technique for targeting calcium in PrCa. Recently, studies performed on PrCa samples have shown that calcium-sensing receptor regulates cytoplasmic calcium levels in relation to extracellular calcium concentrations. Recent publications have also revealed the role of BAP1 and FBXL2 associated endoplasmic reticular IP3Rs in controlling the trafficking of calcium from cytosol into the mitochondria of PrCa cells. Competitive binding between BAP1, PTEN and FBXL2 to IP3Rs regulates the calcium flux of mitochondria and thereby controls apoptosis. Analysis of data released by Prostate Adenocarcinoma (Provisional TCGA) reveals that calcium related proteins play critical role in the development of PrCa. From this constantly expanding appreciation for the role of calcium outside the muscle, we predict that calcium-induced-calcium-release ryanodine receptors could also be involved in determining cell fate.http://link.springer.com/article/10.1186/s13578-018-0217-3Prostate cancerCaSRRyRIP3RBAP1FBXL2 |
spellingShingle | Liyang Wang MengMeng Xu Zhongguang Li Mengting Shi Xin Zhou Xinnong Jiang Joseph Bryant Steven Balk Jianjie Ma William Isaacs Xuehong Xu Calcium and CaSR/IP3R in prostate cancer development Cell & Bioscience Prostate cancer CaSR RyR IP3R BAP1 FBXL2 |
title | Calcium and CaSR/IP3R in prostate cancer development |
title_full | Calcium and CaSR/IP3R in prostate cancer development |
title_fullStr | Calcium and CaSR/IP3R in prostate cancer development |
title_full_unstemmed | Calcium and CaSR/IP3R in prostate cancer development |
title_short | Calcium and CaSR/IP3R in prostate cancer development |
title_sort | calcium and casr ip3r in prostate cancer development |
topic | Prostate cancer CaSR RyR IP3R BAP1 FBXL2 |
url | http://link.springer.com/article/10.1186/s13578-018-0217-3 |
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