Switching off RAD51 may enhance the effect of radiotherapy
A team led by Dr Susan Short from University of Leeds has found that switching off a protein that helps repair DNA damage can sensitize glioblastoma cells to radiotherapy. The study results have been published in Stem Cell Reports.
The protein, called RAD51, plays a central role in the repair of DNA double-strand breaks. Previous studies have linked it to glioblastoma and numerous other cancers.
Patients with glioblastoma tend to have poor prognosis despite surgery and high-dose radiotherapy. This is in part because glioblastoma stem cells in the tumor are able to survive DNA damage caused by radiotherapy and then repopulate the tumor.
In the work, Dr Short and colleagues examined clinical samples and patient-derived glioblastoma stem cells, and confirmed that RAD51 is highly expressed in glioblastoma stem cells. Dr Short explained that radiotherapy damages the DNA in glioblastoma cells but RAD51 helps repair this damaged DNA.
So switching off RAD51 might be a way to sensitize glioblastoma stem cells to radiotherapy, the researchers assumed. To test the hypothesis, they investigated the effect of the combination of small-molecule RAD51 inhibitors and radiation. The results were promising: RAD51 inhibitors combined with radiation promoted loss of stem cells.
Although the RAD51 inhibitors tested in the study are not suitable to be used in humans, the study provides a new treatment method for glioblastoma.
Glioblastoma is a rapidly growing, aggressive tumor in the central nervous system. Common treatments include surgery, radiotherapy, chemotherapy, and targeted therapy. Despite these treatment options, the survival rate of the disease is still too low -- the median survival is less than 18 months. The poor prognosis of glioblastoma is due to its complexity, its location in the brain, treatment side effects, drug resistance, and many other factors. It is required to develop better, safer drugs.
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