E2f6, a member of the E2F transcription factor family, is involved in regulating a wide variety of genes through activation and repression. It is associated with pathways such as the E2F/Rb pathway, which is crucial for cell growth, differentiation, and death. E2f6 has significance in embryonic development, cell viability, and apoptosis, making it of great biological importance [3]. Genetic models are valuable for studying its functions.

In mouse development, E2f6, part of the polycomb repressive complex 1.6 (PRC1.6), is essential for targeting and initiating epigenetic silencing of germline genes in early embryogenesis. Inactivation of E2f6 leads to failure in depositing CpG island DNA methylation at these genes during implantation [1]. In breast cancer cells, RNA interference-mediated depletion of E2f6 reduces cell viability, especially during replication stress, suggesting it could be a target for combined therapy [2]. Also, in gastric carcinoma, down-regulation of E2f6 suppresses cell proliferation and invasion, and promotes apoptosis [4].

In conclusion, E2f6 plays a vital role in epigenetic silencing during embryonic development. In disease conditions, it impacts cell viability in breast cancer and the progression of gastric carcinoma. The use of gene knockout or conditional knockout mouse models has been instrumental in revealing these functions, providing insights into potential therapeutic targets for related diseases.