Host: The Japan Radiation Research Society, Chairman of the 52nd Annual Meeting, Toshiteru Okubo (Radiation Effects Research Foundation)
Homologous recombination is critical for DNA double-strand break repair in mitotic cells, and deregulation of the pathway could cause carcinogenesis and alter sensitivity to DNA-damaging agents. Recently, some meiosis-specific proteins involved in homologous recombination are shown to be aberrantly expressed in cancer cells. We assumed that ectopic expression of such proteins in mitotic cells could modulate the intrinsic homologous recombination pathway and alter sensitivity to radiation or DNA-damaging anti-cancer drugs, and have assessed the role of such proteins in mitotic cells. Here we report on the role of the SYCP2 protein in mitotic cells. The SYCE2 protein is a component of the central elements of the synaptonemal complex, a meiosis-specific supramolecular proteinaceous structure that is essential for synapsis of the maternal and paternal homologous chromosomes. While it is not normally expressed in mitotic cells, reverse transcription-polymerase chain reaction analysis revealed that SYCE2 is aberrantly expressed in cells derived from breast cancer and hematopoietic malignancies. Forced expression of SYCE2 in normal epithelial cells conferred resistance to ionizing radiation. Radiation-induced focus formation of Rad51 was increased in SYCE2-expressing cells. These findings suggest that SYCE2 induces resistance to radiation by modulating the intrinsic Rad51-dependent homologous recombination pathway in cancer cells.
