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Cancer cells' DNA repair disrupted to increase radiation sensitivity
Date:12/1/2011

ding, reaching a condition called senescence. If this first cell-cycle "stop sign" is bypassed, cells continue dividing until telomeres become critically short and reach a second stopping point, when most cells die. In rare instances, cells bypass this second "stop sign" and survive. This survival is often associated with telomerase activation and the onset of cancer.

This was the basis for experiments Drissi and his colleagues conducted to compare the radiation sensitivity and survivability of cells based on telomere length. They also monitored DNA repair responses in the cells by looking for specific biochemical signs that indicate whether the repair systems are working.

The tests involved normal human foreskin cells called fibroblasts and human cervical carcinoma cells. They exposed the cells to ionizing radiation and analyzed DNA repair responses as telomeres became progressively shorter. In the cervical cancer cells, researchers blocked the telomerase enzyme before radiation treatment to induce progressively shorter telomeres.

Both late-stage noncancerous cells with shorter telomeres, and cancer cells with induced shorter telomeres, were more radiosensitive and died more quickly, according to the study.

Among cancer cells with maintained telomere length, close to 10 percent receiving the maximum dose of ionizing radiation used in the study (8 Gy, or Gray Units) survived the treatment. None of the cancer cells with the shortest telomeres survived that exposure.

Researchers said the cancer cells became more radiosensitive because material inside the chromosomes called chromatin compacted as telomeres became shorter. Compacted chromatin then disrupted the biochemical signaling of a protein called ATM (ataxiatelangeietasia mutated).

ATM is a master regulator of DNA repair and cell division. It sends signals to activate other biochemical targets (H2AX, SMC1, NBS1 and p53) that help direct DNA repair and pr
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Contact: Nick Miller
nicholas.miller@cchmc.org
513-803-6035
Cincinnati Children's Hospital Medical Center
Source:Eurekalert

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