Carcinogenesis is a multistage process resulting from a cumulative malfunctioning of DNA replication, double-strand break (DSB) repair, and immune signaling. Chronic stimulation of the innate immune system can cause tumorigenesis. Our lab is interested in understanding the functions of DNA repair and replication factors in the innate immune response.
We have recently reported a novel role of RAD51 in immunity in addition to its known functions in DSB repair and replication-fork processing. We discovered that the downregulation of RAD51 leads to the upregulation of the innate immune response pathway genes upon radiation-induced DNA damage and replication stress.
Currently, we are investigating the involvement of a number of DNA repair and replication factors in the suppression of the innate immune response and carcinogenesis. Our long-term goal is to exploit innate immune response signaling triggered by DSB repair factor-defects and to utilize the existing immune system to kill tumor cells.