Host: The Japan Radiation Research Society
Co-host: Asian Association for Radiation Research
Radiation is one of the major treatment modes for cancer therapy. However, exposure of tumor cells to radiation as well as anticancer drugs, both of which are DNA-damaging agents, leads to cellular responses to repair DNA. The DNA repair has a critical role for tumors to cope with DNA damage and to survive genotoxic stress. When DNA is broken, two-pathways are effective for the double-strand break repair. One is non-homologous endjoining at the G0 and G1 phases of the cell cycle and another is homologous recombination at the S phase of the cell cycle. We focused on the latter mechanism, where Rad51 plays a critical role for homology search and strand exchange. We investigated the effect of RNAi of Rad51 gene in cancer cells to their radiosensitivity. The double stranded short RNA (small interfering RNA) of Rad51 were synthesized and transfected by use of lipofectamine to mouse teratocarcinoma F9 cells and HeLa cells. The Western blot showed that the amount of RAD51 protein in cells transfected withRad51 siRNA was greatly reduced to about 16 % to that of cells transfected with control or scrabled siRNAs. In addition, the F9 teratocarcinoma cells transfected with Rad51 siRNA became much more sensitive to X-irradiation at 6 Gy. The Rad51 siRNA transfected F9 cells also became more sensitive to cisplatin. This method can be applied to cancer radiotherapy and chemotherapy to minimize the doses of radiation or anticancer drugs, which usually are thought to exert their effects by breaking double-stranded DNA.
