TRPM4 channel and cancer. (10th July 2019)
- Record Type:
- Journal Article
- Title:
- TRPM4 channel and cancer. (10th July 2019)
- Main Title:
- TRPM4 channel and cancer
- Authors:
- Gao, Yahui
Liao, Ping - Abstract:
- Abstract: The TRPM4 channel has been extensively studied in cerebral diseases such as stroke, head injury and multiple sclerosis. In the heart, gain-of-function mutations of TRPM4 are a cause of familial cardiac block. Recently, evidence has emerged to support the role of TRPM4 in certain types of cancer, such as prostate cancer and large B cell lymphoma. The expression of TRPM4 could mediate certain behaviors of cancer cells such as migration and invasion. However, the mechanisms are largely unknown. As a nonselective monovalent cation channel, TRPM4 upregulation and activation enhance sodium entry, which leads to depolarization of the membrane potential. The membrane potential is critical in regulating calcium influx, and a disturbed calcium homeostasis is always associated with cancer cell behaviors. Research on TRPM4 channels in cancer is at a very early stage. In this review, we summarize the expression of TRPM4 in various cancers as well as our current understanding of TRPM4 in cancer. The potential mechanisms of the TRPM4 channel in regulating calcium homeostasis in cancer cells are further discussed in detail. Targeting the TRPM4 channel can be a novel way of managing cancer metastasis via disrupting calcium signaling pathways. Highlights: Upregulation of TRPM4 channel has been reported in prostate cancer and large B cell lymphoma. TRPM4 upregulation is associated with cancer cell migration and invasion. TRPM4 potentially yields its function via regulatingAbstract: The TRPM4 channel has been extensively studied in cerebral diseases such as stroke, head injury and multiple sclerosis. In the heart, gain-of-function mutations of TRPM4 are a cause of familial cardiac block. Recently, evidence has emerged to support the role of TRPM4 in certain types of cancer, such as prostate cancer and large B cell lymphoma. The expression of TRPM4 could mediate certain behaviors of cancer cells such as migration and invasion. However, the mechanisms are largely unknown. As a nonselective monovalent cation channel, TRPM4 upregulation and activation enhance sodium entry, which leads to depolarization of the membrane potential. The membrane potential is critical in regulating calcium influx, and a disturbed calcium homeostasis is always associated with cancer cell behaviors. Research on TRPM4 channels in cancer is at a very early stage. In this review, we summarize the expression of TRPM4 in various cancers as well as our current understanding of TRPM4 in cancer. The potential mechanisms of the TRPM4 channel in regulating calcium homeostasis in cancer cells are further discussed in detail. Targeting the TRPM4 channel can be a novel way of managing cancer metastasis via disrupting calcium signaling pathways. Highlights: Upregulation of TRPM4 channel has been reported in prostate cancer and large B cell lymphoma. TRPM4 upregulation is associated with cancer cell migration and invasion. TRPM4 potentially yields its function via regulating intracellular calcium levels. … (more)
- Is Part Of:
- Cancer letters. Volume 454(2019)
- Journal:
- Cancer letters
- Issue:
- Volume 454(2019)
- Issue Display:
- Volume 454, Issue 2019 (2019)
- Year:
- 2019
- Volume:
- 454
- Issue:
- 2019
- Issue Sort Value:
- 2019-0454-2019-0000
- Page Start:
- 66
- Page End:
- 69
- Publication Date:
- 2019-07-10
- Subjects:
- Migration -- Invasion -- Proliferation -- Ion channels -- Calcium -- Cancer
Cancer -- Periodicals
Neoplasms -- Periodicals
Cancer -- Périodiques
Electronic journals
616.994 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03043835/ ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.canlet.2019.04.012 ↗
- Languages:
- English
- ISSNs:
- 0304-3835
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3046.485000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 20407.xml