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Impaired actin filaments decrease cisplatin sensitivity via dysfunction of volume-sensitive Cl- channels in human

Takahiro Shimizu1, Takuto Fujii1, Hironao Ohtake1

  • 1Department of Pharmaceutical Physiology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.

Journal of Cellular Physiology
|May 7, 2020
PubMed

Insights

Disrupting actin filaments in cancer cells impairs volume-sensitive outwardly rectifying (VSOR) chloride channels. This dysfunction leads to resistance against cisplatin chemotherapy in human epidermoid carcinoma cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Cisplatin is a crucial chemotherapy agent, but cancer cells develop resistance.
  • Loss of volume-sensitive outwardly rectifying (VSOR) chloride channels is linked to cisplatin resistance.

Purpose of the Study:

  • To investigate the role of actin filaments and VSOR channels in cisplatin resistance of human epidermoid carcinoma cells.

Main Methods:

  • Compared protein expression and actin filament organization in cisplatin-sensitive (KB) and resistant (KCP-4) cells.
  • Utilized β-actin knockdown and cytochalasin D treatment to disrupt actin filaments.
  • Assessed VSOR chloride currents and the regulatory volume decrease (RVD) process.

Main Results:

  • KB cells showed higher β-actin expression and more organized actin filaments than KCP-4 cells.
  • β-actin knockdown and cytochalasin D treatment reduced VSOR currents and slowed RVD.
  • Cytochalasin D also inhibited cisplatin-induced apoptosis in KB cells.

Conclusions:

  • Disruption of actin filaments leads to VSOR channel dysfunction.
  • VSOR channel dysfunction contributes to cisplatin resistance in human epidermoid carcinoma cells.
Keywords:
actin filamentsapoptosiscell volumechloride channelscisplatin

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