E2f1, a member of the E2F family of transcription factors, is a central player in cell cycle progression. It regulates the transcription of S phase cyclins and genes essential for DNA replication, DNA repair, and apoptosis [1,2,4]. E2f1 is involved in multiple signaling pathways, and its activity is tightly controlled by DNA damage checkpoints. Altered tumor suppressor and oncogenic signaling often interfere with E2F1 regulation, making it relevant in cancer research [1]. Genetic models, such as knockout (KO) mouse models, are valuable tools for studying E2f1's functions.

Knock-in mouse models have demonstrated the importance of E2F1 post-translational modifications in regulating DNA repair and physiological responses to DNA damage. E2F1 can recruit histone acetyltransferases and other proteins to sites of DNA damage, promoting repair in a transcription-independent manner [3]. In the context of cancer, E2F1 is highly expressed in many tumor tissues and cells, playing a role as a cancer-promoting gene. Its up-regulation is related to tumor occurrence, development, metastasis, and prognosis, making it a potential target for cancer treatment [2].

In conclusion, E2F1 is crucial for cell cycle regulation, DNA repair, and apoptosis. Model-based research, especially using KO mouse models, has revealed its roles in DNA repair and cancer-related processes. Understanding E2F1's functions contributes to a better understanding of normal biological processes and provides potential strategies for cancer treatment.