Stokłosa, Paulina; Kappel, Sven; Peinelt, Christine (2022). A Novel Role of the TRPM4 Ion Channel in Exocytosis. Cells, 11(11) MDPI 10.3390/cells11111793
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Under physiological conditions, the widely expressed calcium-activated TRPM4 channel conducts sodium into cells. This sodium influx depolarizes the plasma membrane and reduces the driving force for calcium entry. The aberrant expression or function of TRPM4 has been reported in various diseases, including different types of cancer. TRPM4 is mainly localized in the plasma membrane, but it is also found in intracellular vesicles, which can undergo exocytosis. In this study, we show that calcium-induced exocytosis in the colorectal cancer cell line HCT116 is dependent on TRPM4. In addition, the findings from some studies of prostate cancer cell lines suggest a more general role of TRPM4 in calcium-induced exocytosis in cancer cells. Furthermore, calcium-induced exocytosis depends on TRPM4 ion conductivity. Additionally, an increase in intracellular calcium results in the delivery of TRPM4 to the plasma membrane. This process also depends on TRPM4 ion conductivity. TRPM4-dependent exocytosis and the delivery of TRPM4 to the plasma membrane are mediated by SNARE proteins. Finally, we provide evidence that calcium-induced exocytosis depends on TRPM4 ion conductivity, not within the plasma membrane, but rather in TRPM4-containing vesicles.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Biochemistry and Molecular Medicine |
UniBE Contributor: |
Stoklosa, Paulina Agnieszka, Kappel, Sven, Peinelt, Christine |
Subjects: |
500 Science > 570 Life sciences; biology 600 Technology > 610 Medicine & health |
ISSN: |
2073-4409 |
Publisher: |
MDPI |
Language: |
English |
Submitter: |
Pubmed Import |
Date Deposited: |
13 Jun 2022 09:23 |
Last Modified: |
05 Dec 2022 16:20 |
Publisher DOI: |
10.3390/cells11111793 |
PubMed ID: |
35681487 |
Uncontrolled Keywords: |
TRPM4 cancer cell exocytosis |
BORIS DOI: |
10.48350/170594 |
URI: |
https://boris.unibe.ch/id/eprint/170594 |