Abstract
Homologous recombination is an essential mechanism in mitosis and meiosis. Meiosis-specific proteins are not expressed in normal somatic cells. However, accumulating evidence suggests that some meiosis-specific proteins, including those involved in homologous recombination, are expressed in tumors of non-germ cell origin. Although these meiosis-specific proteins regulate chromosomal dynamics in meiotic cells, their role in somatic cells is unknown. Here we show that the meiosis-specific synaptonemal complex protein SYCP3 was ectopically expressed in human cancers from various tissue origins, and induced aneuploidy and hypersensitivity to ionizing radiation in immortalized epithelial cells. In somatic cells expressing SYCP3, increases in gamma-H2AX foci and a decrease in radiation-induced Rad51 foci formation were observed. These observations suggest that aberrant expression of SYCP3 in somatic cells might induce chromosome instability and hypersensitivity to ionizing radiation by prohibiting the intrinsic homologous recombination pathway.
