Dequalinium induces cell death in human leukemia cells by early mitochondrial alterations which enhance ROS production
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Updated: Jul 17, 2026
Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
Published on: September 5, 2019
Pilar Sancho1, Eva Galeano, Elena Nieto
1Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Campus Universitario, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain.
Abstract:
Dequalinium (DQA) has been proposed as a selective antitumoral agent due to its preferential accumulation in mitochondria of cancer cells. Our aim was a better understanding of DQA cytotoxicity. DQA-induced NB4 and K562 cell alterations are initiated within the first 30 min of treatment at a high DQA concentration with a mitochondrial membrane depolarization. Cytochrome c release to cytoplasm, superoxide anion overproduction and ATP depletion in NB4 cells induce, 16 h later, apoptosis by a typical caspase-9/caspase-3-dependent intrinsic pathway. K562 cells were more resistant to the DQA effect than NB4 cells, remaining viable for longer time periods.
Insights
Dequalinium (DQA) shows selective cancer cell toxicity by disrupting mitochondria. NB4 cells undergo apoptosis via intrinsic pathways, while K562 cells exhibit greater resistance to DQA treatment.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Dequalinium (DQA) is investigated as a potential antitumoral agent.
- DQA exhibits preferential accumulation in cancer cell mitochondria.
Purpose of the Study:
- To elucidate the mechanisms underlying Dequalinium (DQA) cytotoxicity.
- To understand the differential response of cancer cell lines to DQA.
Main Methods:
- Treatment of NB4 and K562 cancer cell lines with DQA.
- Monitoring of mitochondrial membrane potential, cytochrome c release, superoxide anion production, and ATP levels.
- Assessment of apoptosis induction via caspase-9/caspase-3 dependent pathways.
Main Results:
- DQA rapidly induced mitochondrial membrane depolarization in NB4 and K562 cells within 30 minutes at high concentrations.
- NB4 cells exhibited apoptosis, characterized by cytochrome c release, superoxide overproduction, and ATP depletion, mediated by the intrinsic caspase pathway.
- K562 cells demonstrated higher resistance to DQA compared to NB4 cells, with prolonged viability.
Conclusions:
- DQA induces cytotoxicity through mitochondrial dysfunction and intrinsic apoptosis pathway activation.
- Cancer cell line sensitivity to DQA varies, with NB4 cells being more susceptible than K562 cells.
- DQA's selective mitochondrial targeting offers potential for targeted cancer therapy development.
