TY - JOUR
T1 - Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells
AU - Hung, Te Yu
AU - Huang, Huai Ying Ingrid
AU - Wu, Sheng Nan
AU - Huang, Chin Wei
N1 - Funding Information:
This study was supported in part by the National Cheng Kung University (D106-35A13, D107-F2519 and NCKUH-10709001 to SNW), Tainan City, Taiwan. SNW received a Talent Award for Outstanding Researchers from the Ministry of Education, Taiwan. This work was also supported in part by grants from the Ministry of Science and Technology, Taiwan (107–2314-B-006-018-, 107–2320-B-006-019-, 108–2320-B-006-023-, 109–2314-B-006 -034 -MY3 to CWH), and the National Cheng Kung University Hospital (20180254, 20190160 to CWH). The funding bodies did not play any roles in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/12
Y1 - 2021/12
N2 - Background: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods: With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13–06-MG. Results: In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13–06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions: The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.
AB - Background: Vigabatrin (VGB) is an approved non-traditional antiepileptic drug that has been revealed to have potential for treating brain tumors; however, its effect on ionic channels in glioma cells remains largely unclear. Methods: With the aid of patch-clamp technology, we investigated the effects of VGB on various ionic currents in the glioblastoma multiforme cell line 13–06-MG. Results: In cell-attached configuration, VGB concentration-dependently reduced the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) counteracted the VGB-induced inhibition of IKCa channels. However, the activity of neither large-conductance Ca2+-activated (BKCa) nor inwardly rectifying K+ (KIR) channels were affected by the presence of VGB in human 13–06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl2 effectively suppressed BKCa and KIR channels. Conclusions: The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.
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U2 - 10.1186/s40360-021-00472-3
DO - 10.1186/s40360-021-00472-3
M3 - Article
C2 - 33441172
AN - SCOPUS:85099372416
SN - 2050-6511
VL - 22
JO - BMC pharmacology & toxicology
JF - BMC pharmacology & toxicology
IS - 1
M1 - 6
ER -