Related Experiment Video
Updated: Jan 13, 2026
09:43
Measurement of Heme Synthesis Levels in Mammalian Cells
Published on: July 9, 2015
12.5K
When heme is low, copper kills cancer.
1Department of Medicine V, University Medical Centre Mannheim, University of Heidelberg, Mannheim, Germany; Department of Internal Medicine 3, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Dresden, Germany; Division of Nephrology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.
Cell
|January 9, 2026
Summary
Low heme levels destabilize respiratory chain complex IV, releasing copper and inducing cell death via cuproptosis in acute myeloid leukemia. This finding reveals a novel mechanism for targeting cancer cells.
Area of Science:
- Biochemistry
- Cell Biology
- Cancer Research
Background:
- Heme is essential for oxygen transport and redox reactions.
- Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow.
- Cuproptosis is a copper-dependent cell death pathway.
Purpose of the Study:
- To investigate the role of heme in regulating mitochondrial function and cell death in AML.
- To elucidate the mechanism by which low heme concentrations affect cancer cells.
Main Methods:
- The study by Lewis and Gruber et al. utilized biochemical assays to analyze mitochondrial respiratory chain complexes.
- Cellular models of acute myeloid leukemia were employed to study cell viability and death pathways.
- Copper levels and the process of cuproptosis were specifically monitored.
Main Results:
- Low concentrations of heme were found to destabilize complex IV of the respiratory chain.
- This destabilization led to the release of copper within the cell.
- The released copper triggered a potent form of cell death known as cuproptosis in AML cells.
Conclusions:
- Heme concentration is a critical regulator of mitochondrial integrity and cell fate.
- Targeting heme metabolism or copper-induced cuproptosis presents a potential therapeutic strategy for AML.
- This research uncovers a novel vulnerability in acute myeloid leukemia cells exploitable for treatment.
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