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The human genome is constantly exposed to both endogenous and exogenous stresses, which can lead to errors in DNA replication and the accumulation of DNA mutations, thereby increasing the risk of cancer development. The transcription factor E2F1 is a key regulator of DNA repair. E2F1 also has defined roles in the replication of many cell cycle-related genes and is highly expressed in cancer cells, and its abundance is strongly associated with poor prognosis in cancers. Studies on colon cancer have demonstrated that the depletion of E2F1 leads to reduced levels of homologous recombination (HR), resulting in interrupted DNA replication and the subsequent accumulation of DNA lesions. Our results demonstrate that the depletion of E2F1 also causes reduced RAD51-mediated DNA repair and diminished cell viability resulting from DNA damage. Furthermore, the extent of RAD51 and RPA colocalization is reduced in response to DNA damage; however, RPA single-stranded DNA (ssDNA) nucleofilament formation is not affected following the depletion of E2F1, implying that ssDNA gaps accumulate when RAD51-mediated DNA gap filling or repair is diminished. Surprisingly, we also demonstrate that E2F1 forms foci with RAD51 or RPA at DNA break sites on damaged DNA. These findings provide evidence of a molecular mechanism underlying the E2F1-mediated regulation of HR activity and predict a fundamental shift in the function of E2F1 from regulating cell division to accelerating tumor development.

E2F1 facilitates DNA break repair by localizing to break sites and enhancing the expression of homologous recombination factors