scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2020 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract 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.

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2021 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract 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.

scholarly journals Depressive effectiveness of vigabatrin (γ-vinyl-GABA), an antiepileptic drug, in intermediate-conductance calcium-activated potassium channels in human glioma cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract 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.

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2021 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Ionic Channels ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying

Abstract 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.

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2020 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Human Glioma Cells ◽  
Subsequent Application ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying ◽  
Ionic Effects

Abstract Background Vigabatrin (VGB, y-vinyl-GABA) is an approved non-traditional antiepileptic drug that has been revealed to have the therapeutic propensity for brain tumors; however, its ionic effects in glioma cells remain unclear to a large extent. 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, addition of VGB concentration-dependently lessened the activity of intermediate-conductance Ca2+-activated K+ (IKCa) channels, while subsequent application of DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) thwarted the VGB-induced inhibition of IKCa channels. Neither the activity of large-conductance Ca2+-activated (BKCa) nor that of inwardly rectifying K+ (KIR) channels was adjusted 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. Conclusion The inhibitory effect of VGB on IKCa channels demonstrated in the current study could be an unidentified but important underlying mechanism of VGB-induced antineoplastic (e.g., anti-glioma) actions.

scholarly journals Depressive Effectiveness of Vigabatrin (y-Vinyl-GABA), an Antiepileptic Drug, in Intermediate-conductance Calcium-Activated Potassium Channels in Human Glioma Cells

2020 ◽  
Author(s):  
Te-Yu Hung ◽  
Huai-Ying Ingrid Huang ◽  
Sheng-Nan Wu ◽  
Chin-Wei Huang
Keyword(s):  
Antiepileptic Drug ◽  
Glioma Cells ◽  
Ionic Currents ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Ca Channels ◽  
Human Glioma Cells ◽  
Calcium Activated Potassium Channels ◽  
Inwardly Rectifying ◽  
Ionic Effects

Abstract Background: Vigabatrin (VGB, y-vinyl-GABA) is an approved non-traditional antiepileptic drug that has been revealed to have the therapeutic propensity for brain tumors; however, its ionic effects in glioma cells remain unclear to a large extent.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, addition of VGB concentration-dependently lessened the activity of intermediate-conductance Ca 2+ -activated K + (IK Ca ) channels, while subsequent application of DCEBIO (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one) thwarted the VGB-induced inhibition of IK Ca channels. Neither the activity of large-conductance Ca 2+ -activated (BK Ca ) nor that of inwardly rectifying K + (K IR ) channels was adjusted by the presence of VGB in human 13-06-MG cells. However, in the continued presence of VGB, the addition of GAL-021 or BaCl 2 effectively suppressed BK Ca and K IR channels.Conclusion: The inhibitory effect of VGB on IK Ca channels demonstrated in the current study could be an unidentified but important underlying mechanism of VGB-induced antineoplastic ( e.g. , anti-glioma) actions.

scholarly journals Inhibition of cell proliferation by 2-fluorobenzaldehyde retinoic acid conjugate through suppression of STAT3 activation in human glioma cells

2015 ◽  
Vol 10 (4) ◽  
pp. 966
Author(s):  
Ji-Heng Hao ◽  
Dian-Feng Hu ◽  
Li-Mei Mao ◽  
Shi-Gang Zhang ◽  
Ji-Yue Wang ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Glioma Cells ◽  
Inhibitory Effect ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Expression Of Genes ◽  
Acid Conjugate ◽  
G0 Phase ◽  
Induced Apoptosis ◽  
Endothelial Growth Factor

<p class="Abstract">The present study was performed to investigate the effect of 2-fluorobenzaldehyde retinoic acid conjugate on activation of STAT3 pathway in human glioma cells. The results revealed that the compound exhibited inhibitory effect on the activation of STAT3 induced constitutively and by interleukin-6. The inhibitory effect on STAT3 activation was found to be concentration- and time-dependent. In U373 glioma cells, 2-fluorobenzaldehyde retinoic acid conjugate treatment caused a significant enhancement in the expression of proapoptotic proteins like Bax and Bak. Its treatment inhibited the expression of genes including, cyclin D1, Bcl-2, Bcl-xL, survivin, Mcl-1, and vascular endothelial growth factor (VEGF) in U373 glioma cells. Furthermore, the conjugate inhibited proliferation, induced apoptosis and caused accumulation of cells in G1-G0 phase of cell cycle. Thus, 2-fluorobenzaldehyde retinoic acid conjugate acts as a potent inhibitor of STAT3 activation that can be promising importance for the prevention and treatment of gliomas.</p><p> </p>

Underlying Mechanism of Quercetin-induced Cell Death in Human Glioma Cells

2008 ◽  
Vol 33 (6) ◽  
pp. 971-979 ◽  
Author(s):  
Eui Joong Kim ◽  
Chang Hwa Choi ◽  
Ji Yeon Park ◽  
Soo Kyung Kang ◽  
Yong Keun Kim
Keyword(s):  
Cell Death ◽  
Glioma Cells ◽  
Underlying Mechanism ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals MicroRNA-302c enhances the chemosensitivity of human glioma cells to temozolomide by suppressing P-gp expression

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
YiHan Wu ◽  
Yuan Yao ◽  
YongLi Yun ◽  
MeiLing Wang ◽  
RunXiu Zhu
Keyword(s):  
Glioma Cells ◽  
Inverse Correlation ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glycoprotein P ◽  
P Glycoprotein

Abstract Increasing evidence indicates that microRNAs (miRNAs) participate in the regulation of chemoresistance in a variety of cancers including glioma. However, the molecular mechanism underlying the development of chemoresistance in glioma is not well understood. The aim of the present study was to explore the role of miRNAs in the chemosensitivity of glioma cells and the underlying mechanism. By microarray and qRT-PCR, we observed significant down-regulation of microRNA-302c (miR-302c) in the temozolomide (TMZ)-resistant human glioma tissues/cells. The low expression of miR-302c was closely associated with poor prognosis and chemotherapy resistant in patients. miR-302c up-regulation re-sensitized U251MG-TMZ cells and LN229-TMZ cells to TMZ treatment, as evidenced by inhibition of the cell viability, cell migration, and invasion capacity, and promotion of the apoptosis after TMZ treatment. Furthermore, P-glycoprotein (P-gp) was identified as a functional target of miR-302c and this was validated using a luciferase reporter assay. In addition, P-gp was found to be highly expressed in U251MG-TMZ cells and there was an inverse correlation between P-gp and miR-302c expression levels in clinical glioma specimens. Most importantly, we further confirmed that overexpression of P-gp reversed the enhanced TMZ-sensitivity induced by miR-302c overexpression in U251MG-TMZ and LN229-TMZ cells. Our finding showed that up-regulation of miR-302c enhanced TMZ-sensitivity by targeting P-gp in TMZ-resistant human glioma cells, which suggests that miR-302c would be potential therapeutic targets for chemotherapy-resistant glioma patients.

Sign in / Sign up

Export Citation Format

Share Document