More than 1 million people in the United States are diagnosed with skin cancer each year. In the new study, researchers examined a type of skin cancer, called squamous cell carcinoma, which accounts for between 200,000 and 300,000 new cases per year.
Sunlight can damage a skin cell's DNA. Normally, a protein called protein kinase C (PKC) is activated in response to the damage. If the damage is too great to repair, the PKC protein directs the cell to die.
Healthy cells grow and divide in a cell-division cycle. At several checkpoints in this cycle, the cell stops to repair damaged DNA before progressing to the next step in the cycle. The new study found that the PKC gene is responsible for stopping the cell at the checkpoint just before the point when the cell divides. In squamous cell carcinoma, the PKC gene is turned off. The cell proceeds to divide without first stopping to repair its DNA, thus producing daughter tumor cells.
Denning said a class of drugs called protein kinase inhibitors potentially could shrink tumors by turning the PKC gene back on. Several such drugs have been approved by the Food and Drug Administration for other cancers. Denning is pursuing grant funding to test such drugs on animal models.
Citation: Edward L. LaGory, Leonid A. Sitailo, Mitchell F. Denning, 'The Protein Kinase Cδ Catalytic Fragment Is Critical for Maintenance of the G2/M DNA Damage Checkpoint', Journal of Biological Chemistry, 285, 1879-1887; doi: 10.1074/jbc.M109.055392
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