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Recombinant Methioninase as a DNA Demethylation Agent
Robert M Hoffman1,2, David Machover3
1AntiCancer, Inc., San Diego, CA, USA. all@anticancer.com.
Methods in Molecular Biology (Clifton, N.J.)
|February 7, 2019
Summary
Methionine restriction using recombinant methioninase (rMETase) significantly reduces DNA methylation in human cancer cells. This epigenetic modification by rMETase shows promise as a cancer therapy strategy.
Area of Science:
- Biochemistry
- Epigenetics
- Cancer Biology
Background:
- DNA methylation is a critical epigenetic mechanism involved in gene regulation.
- Aberrant DNA methylation patterns are hallmarks of many cancers.
- Methionine restriction is a potential strategy to modulate epigenetic processes in cancer cells.
Purpose of the Study:
- To investigate the impact of methionine restriction, induced by recombinant methioninase (rMETase), on DNA methylation in human cancer cells.
- To compare the DNA hypomethylating effects of rMETase with a known DNA methyltransferase inhibitor.
Main Methods:
- Treatment of CCRF-CEM human cancer cells with rMETase under subcytotoxic conditions.
- Quantification of genomic DNA methylation using [3H]methyl-S-adenosylmethionine incorporation.
- Analysis of DNA methylation changes via methylation-sensitive arbitrarily-primed PCR.
Main Results:
- rMETase treatment led to significantly lower levels of genomic methylated DNA in cancer cells compared to controls.
- The observed DNA hypomethylation was comparable in extent to that induced by 5-azacytidine, a DNA methyltransferase inhibitor.
Conclusions:
- Recombinant methioninase effectively induces DNA hypomethylation in cancer cells.
- Methionine restriction via rMETase represents a potential therapeutic approach for epigenetic modulation in cancer treatment.
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