FRIDAY, July 7, 2006 (HealthDay News) -- In a finding that could advance the fight against cancer, scientists say a protein called histone H2AX -- which usually repairs severed DNA molecules -- can also join forces with another protein to destroy DNA in damaged cells, triggering cell death.
This natural process occurs when cells are damaged -- for example, from ultraviolet light. H2AX seems to allow the damaged cell to undergo programmed cell death ("apoptosis") before it can become dysfunctional or cancerous, the University of Minnesota researchers explained. They also found that two cellular processes need to be set in motion before H2AX and the other enzyme team up to chop up a cell's DNA and trigger apoptosis.
Learning more about how apoptosis occurs may help scientists find ways to harness the process in order to kill cancer cells or other unwanted tissue, the researchers said.
The study appears in the July 7 issue of the journal Archives of Internal Medicine.
"In the past, people thought histones were just for packaging DNA," lead investigator Zigang Dong said in a prepared statement. "People believe H2AX plays a role in DNA repair. But we find that if DNA can't be repaired, the cell undergoes apoptosis. The histone H2AX is probably important for both apoptosis and DNA repair."
In this study, Dong and his colleagues exposed cells from the skin of mice to damaging amounts of UV light and found that a form of an enzyme called JNK activates both of the cellular processes that lead to DNA destruction.
In one process, JNK initiates a chain reaction that results in the activation of an enzyme that chops up DNA, the researchers said. In the second process, JNK activates H2AX, which works with the activated enzyme to destroy the DNA. This is the first study to show that activation of H2AX is necessary for apoptosis to occur by means of the DNA-chopping enzyme.
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To learn more about DNA, visit the Cold Spring Harbor Laboratory.
