https://orcid.org/0000-0001-6539-5152
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ABSTRACT
Gliomas are the most common type of primary brain tumor. Despite advances in treatment, it remains one of the most aggressive and deadly tumor of the central nervous system (CNS). Gliomas are characterized by high malignancy, heterogeneity, invasiveness, and high resistance to radiotherapy and chemotherapy. It is urgent to find potential new molecular targets for glioma. The TRPM channels consist of TRPM1-TPRM8 and play a role in many cellular functions, including proliferation, migration, invasion, angiogenesis, etc. More and more studies have shown that TRPM channels can be used as new therapeutic targets for glioma. In this review, we first introduce the structure, activation patterns, and physiological functions of TRPM channels. Additionally, the pathological mechanism of glioma mediated by TRPM2, 3, 7, and 8 and the related signaling pathways are described. Finally, we discuss the therapeutic potential of targeting TRPM for glioma.
KEY POINTS
•TRPM channels are widely expressed in the human body and play an important role in gliomas.
• Abnormal expression of TRPM2, 3, 7, and 8 channels in gliomas is associated with disease severity and prognosis.
•TRPM2, 3, 7, and 8 channels are effective targets in glioma.
Abbreviations
| CNS | = | central nervous system |
| TRP | = | transient receptor potential |
| TRPM | = | transient receptor potential melastatin |
| cADPR | = | cyclic ADPR |
| NAD | = | nicotinamide adenine dinucleotide |
| NAAD | = | nicotinate adenine dinucleotide |
| NAADP | = | NAAD-phosphate |
| RNS | = | reactive nitrogen |
| MAPKs | = | mitogen-activated protein kinases |
| PKC | = | protein kinase C |
| PLC | = | phospholipase C |
| ER | = | endoplasmic reticulum |
| GBM | = | glioblastoma multiforme |
| Se | = | selenium |
| miRNAs | = | MicroRNAs |
| CSCs | = | cancer stem cells |
| MRE | = | miRNA recognition element |
| EMT | = | epithelial-to-mesenchymal transformation |
| PS | = | pregnenolone sulfate |
| ALDH1 | = | aldehyde dehydrogenase 1 |
| GSC | = | glioma stem cell |
| CaMKII | = | Ca2+/calmodulin-dependent protein kinase II |
| LSCC | = | laryngeal squamous cell carcinoma |
| DTX | = | docetaxel |
| VQ-1 | = | Vacquinol-1 |
| VEGF | = | vascular endothelial growth factor |
| PIP2 | = | phosphatidylinositol 4,5-bisphosphate |
| ADPR | = | ADP-ribose |
| CAM | = | calmodulin |
| TNFα | = | tumor necrosis factor-α |
| RNS | = | reactive nitrogen |
| PKC | = | protein kinase C |
Acknowledgments
We thank all participants of this study.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Author contributions
Z.C., H.X. and J.L. wrote the main manuscript text, E.F., J.Z., R.H., Y.X. and H.W. prepared figures. E.B. and D.S. conceived and designed the study. All authors reviewed the manuscript.
Ethical approval
This is a review, and there is no ethical conflict.