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Optimized Transfection Strategy for Expression and Electrophysiological Recording of Recombinant Voltage-Gated Ion Channels in HEK-293T Cells
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Suppression of chloride voltage-gated channel 3 expression increases sensitivity of human glioma U251 cells to

Yihe Zhang1,2, Lei Zhou3, Juanjuan Zhang1

  • 1Department of Pathophysiology, Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

Oncology Letters
|July 3, 2018
PubMed

Insights

Suppression of chloride voltage-gated channel 3 (CLCN3) enhances cisplatin

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cisplatin resistance is a significant challenge in glioma treatment.
  • Chloride voltage-gated channel 3 (CLCN3) has been implicated in drug resistance, but its precise role in cisplatin resistance remains unclear.
  • Understanding the mechanisms of cisplatin resistance is crucial for developing effective therapeutic strategies.

Purpose of the Study:

  • To investigate the role of CLCN3 in cisplatin resistance in human glioma U251 cells.
  • To explore the effects of combined cisplatin treatment and CLCN3 suppression on glioma cell viability and apoptosis.
  • To elucidate the underlying mechanisms, particularly lysosomal function, by which CLCN3 influences cisplatin sensitivity.

Main Methods:

  • Human glioma U251 cells were treated with cisplatin alone or in combination with CLCN3 antisense.
  • Cell viability was assessed to determine cytotoxic effects.
  • Apoptosis-related gene expression (TP53, BCL2/BAX ratio) and caspase 3 activation were analyzed.
  • Lysosome stabilization was evaluated in cisplatin-treated cells with and without CLCN3 suppression.

Main Results:

  • CLCN3 suppression significantly decreased the viability of cisplatin-treated U251 cells.
  • Combined treatment enhanced apoptosis, indicated by increased TP53 expression, caspase 3 activation, and a decreased BCL2/BAX ratio.
  • CLCN3 suppression led to decreased lysosome stabilization in cisplatin-treated U251 cells, suggesting lysosomal dysfunction.

Conclusions:

  • CLCN3 suppression sensitizes human glioma cells to cisplatin.
  • The combination of cisplatin and CLCN3 antisense exhibits additive cytotoxic effects.
  • Lysosomal dysfunction induced by CLCN3 suppression is a key mechanism mediating enhanced cisplatin sensitivity in glioma cells.
Keywords:
chloride voltage-gated channel 3cisplatindrug resistancegliomalysosome

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