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Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride

K A Poulsen1, E C Andersen, C F Hansen

  • 1Section of Cell- and Developmental Biology, Department of Biology, The August Krogh Bldg., Univ. of Copenhagen, 13 Universitetsparken, DK-2100, Copenhagen Ø. kapoulsen@bio.ku.dk

American Journal of Physiology. Cell Physiology
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Multidrug-resistant cancer cells resist apoptosis by impairing apoptotic volume decrease (AVD), a process involving cell shrinkage and ion loss. Inhibiting anion channels restores AVD and sensitivity to chemotherapy.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Apoptosis, or programmed cell death, is crucial for development and disease. Cell volume changes and ion flux across the plasma membrane are key events in apoptosis initiation.
  • Ehrlich ascites tumor cells (EATC) provide a model to study apoptosis kinetics. Multidrug resistance (MDR) in cancer cells often involves altered apoptotic pathways.

Purpose of the Study:

  • To investigate the kinetics of apoptotic volume decrease (AVD) and ion content dynamics in wild-type (WT) and multidrug-resistant (MDR) EATC.
  • To elucidate the role of ion movements, particularly NaCl transport, in cisplatin-induced apoptosis and MDR.
  • To assess the impact of anion channel inhibition on AVD and apoptosis in both WT and MDR EATC.

Main Methods:

  • Induction of apoptosis in WT and MDR EATC using cisplatin (5 μM).
  • Monitoring cell volume changes (AVD) and intracellular ion content (Cl-, K+, Na+) over time.
  • Assessing amino acid content and caspase 3 activation.
  • Utilizing the anion channel inhibitor NS3728 to study its effects on AVD and ionic movements.

Main Results:

  • WT EATC exhibited three AVD stages: early water loss (AVD1), partial volume recovery (AVDT), and secondary reduction (AVD2), linked to ion and amino acid loss/gain.
  • MDR EATC showed resistance to cisplatin, with less pronounced AVD1, augmented AVdT, and delayed AVD2, associated with altered NaCl movements and reduced caspase 3 activation.
  • NS3728 inhibited AVD, abolished differences between WT and MDR EATC, and repressed volume-regulated anion channel capacity in MDR EATC.

Conclusions:

  • Impairment of apoptotic volume decrease (AVD), primarily through altered NaCl movements, contributes to cisplatin resistance in MDR EATC.
  • Volume-regulated anion channels play a critical role in AVD and apoptosis, and their dysfunction in MDR EATC confers resistance.
  • Targeting anion channels could be a therapeutic strategy to overcome MDR by restoring apoptotic sensitivity.