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CORM-3 induces DNA damage through Ru(II) binding to DNA
Rhiannon F Lyon1, Hannah M Southam1, Clare R Trevitt1
1School of Biosciences, University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, U.K.
The Biochemical Journal
|June 21, 2022
Summary
The ruthenium complex CORM-3 targets cancer cells by binding to DNA, similar to cisplatin but with a different mechanism. This ruthenium compound induces DNA strand breaks, showing potential as a novel cancer therapeutic.
Area of Science:
- Medicinal Chemistry
- Biochemistry
- Cancer Research
Background:
- CO-releasing molecule-3 (CORM-3) forms ruthenium complexes in water.
- These complexes are internalized by cells and bind to intracellular ligands like thiols, leading to high intracellular Ru(II) concentrations.
Purpose of the Study:
- To investigate the interaction of Ru(II) from CORM-3 with DNA.
- To compare the DNA binding and cellular effects of Ru(II) with cisplatin.
- To assess the potential of CORM-3 as a cancer therapeutic.
Main Methods:
- Cellular uptake and intracellular ligand binding studies.
- DNA binding assays, focusing on guanosine N7 positions.
- Alkaline comet assay to detect DNA strand breaks in colorectal cancer cells.
- Inhibition studies using amino acid-rich growth media.
Main Results:
- Ru(II) binds to exposed guanosine N7 positions on DNA.
- Unlike cisplatin, Ru(II) does not form intramolecular DNA crossbridges but can form intermolecular ones.
- CORM-3 induces DNA strand breaks in human colorectal cancer cells.
- Amino acids in growth media inhibit Ru uptake and subsequent DNA damage.
Conclusions:
- Ruthenium complexes exhibit a distinct mechanism of action compared to platinum-based drugs like cisplatin.
- The observed DNA damage and cytotoxicity suggest Ru(II) is a promising candidate for developing new cancer therapeutics.
- Further research into ruthenium-based compounds is warranted for cancer treatment.
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