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Downregulation of TRPM8 channels induce cell death in human DBTRG glioblastoma cells

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Title Downregulation of TRPM8 channels induce cell death in human DBTRG glioblastoma cells
 
Creator ÖZ, Ahmi
ÇELİK, Ömer
 
Subject Calcium signaling
Cell death
DBTRG cells
Glioblastoma
TRPM8 channels
 
Description 385-392
The calcium ion (Ca2+) is among the most important second messengers for cellular metabolic processes. Cytosolic calcium concentration ([Ca2+]c) is regulated by calcium signals and that are driven by different kinds of cation channels including the Transient Receptor Potential (TRP)channels. The TRPM8cation channels are calcium ion (Ca2+) permeable non-selective cation channels belongs TRP superfamily. The TRPM8 is expressed in central and peripheral nervous system components especially in pain and cold sensation related nerve endings. Glioblastoma is the most potent cancer type of the human brain, and patients has less survival time after the detection of disease. Recently, TRPM8 cation channels involved in several types of cancers including glioblastoma because of high expression levels in cancer tissues. Hence, [Ca2+]c may change depend on TRPM8 activations from extracellular liquid to cytosol and it can be targeted for prevention of cancer progression. Therefore, we have investigated effects of downregulation of TRPM8 cation channels by siRNA transfections and pharmacological blockade of the channels with its specific antagonist on apoptosis and cell viability, intracellular reactive oxygen species production (iROS), mitochondrial membrane depolarization levels (MMD), caspase 3 and caspase 9 enzyme activity values in DBTRG glioblastoma cells. We have found that TRPM8 cation channels has crucial role in cancer progression and uncontrolled cell proliferation, however TRPM8 cation channels’ pharmacologically blockade, or prevention of the channel expression may induce cell death and cellular apoptotic processes. In conclusion, TRPM8 cation channel blockers or downregulation of the channels by genetic manipulations can be useful and potential therapeutic approach against to glioblastoma progression.
 
Date 2023-07-20T06:29:35Z
2023-07-20T06:29:35Z
2023-07
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://nopr.niscpr.res.in/handle/123456789/62306
https://doi.org/10.56042/ijbb.v60i5.950
 
Language en
 
Publisher NIScPR-CSIR,India
 
Source IJBB Vol.60(05) [May 2023]