Table 2.
Ion Channels and Glioma Proliferation/Glioma-related Epilepsy
| Ion Channels and Glioma Proliferation | ||
|---|---|---|
| Ion channel | Ions | Mechanisms/Effects on Proliferation |
| TRPM7 | Ca2+ | Ca2+ influx and activating Ca2+-dependent pathways |
| TRPC6 | Ca2+ | Regulation of cell cycle (G2/M) progression |
| TRPML2 | Ca2+ | Association with Akt/PKB and Erk1/2 pathways |
| Cav3.1, Cav3.2 (voltage-gated Ca2+ channels) | Ca2+ | Ca2+ influx and activation of Ca2+-dependent pathways |
| Kv10.1 (Eag1, Ether-a-go-go-1) | K+ | Involved in modulation of signaling pathways |
| Ether-a-go-go-Related Gene (hERG) | K+ | Involved in modulation of signaling pathways |
| Kv1.5 | K+ | Inversely correlated with increasing glioma grade |
| Kv2.1 | K+ | Regulation of ERK pathway |
| Swelling-induced Cl− channels (VRAC) | Cl− | Promoting gene transcription through signaling pathways |
| CLIC1 (Chloride Intracellular Channel-1) | Cl− | Unclear |
| ANO1 (Anoctamin-1) Ca2+ activated Cl− channel (TMEM16A) | Cl− | Activation of NF-κB signaling pathway |
| ASIC1 and ENaC (Epithelial sodium channel) | Na+ | Regulation of ERK pathway through integrin-β1 |
| Ion Channels and Glioma-related Epilepsy | ||
| Ion channel | Ions/Molecule | Mechanisms/Effect on glioma-related Epilepsy |
| Kir4.1 | K+ | Decreased expression impairs K+ buffering and increase propensity for seizures |
| KCC2 (K+-Cl− cotransporter 2) | K+, Cl− | Altered Cl− homeostasis causes GABAergic disinhibition |
| AQP-4 | H2O | Regulating extracellular potassium concentration and efflux of glutamate |