Cul7, a member of the DOC domain - containing cullin family, encodes an E3 ubiquitin ligase [1,2,5,6,7,9]. It is involved in multiple biological processes such as cell transformation, apoptosis, and ubiquitin - mediated proteolysis [1,2,4,7,9]. It also plays a role in pathways like NF - κB signaling [1,6].

In glioma cells, Cul7 overexpression promotes tumorigenesis via NF - κB activation, while its gene silencing inhibits tumor growth, invasion, and migration both in vitro and in vivo [1]. In colon adenocarcinoma, Cul7 is upregulated and is an independent prognostic factor [4]. In B lymphocytes, Cul7 mediates the degradation of activation - induced cytidine deaminase and regulates Ig class switch recombination [5]. In non - small cell lung cancer, Cul7 - mediated degradation of TET2 leads to EGFR - TKI resistance [6]. In addition, Cul7 promotes cancer cell survival by promoting Caspase - 8 ubiquitination [2]. In the context of retinal degeneration, Cul7 was identified as a therapeutic target, and its suppression protected photoreceptors [3]. Moreover, Cul7 knockout in chondro - tissue specific Cul7 knockout mice affects chondrocyte proliferation and endochondral osteogenesis, with abnormal limb development and growth plate changes [8].

In conclusion, Cul7 has diverse functions in various biological processes and disease conditions. Studies using gene knockout models, such as the chondro - tissue specific Cul7 knockout mice, have revealed its significance in processes like tumorigenesis, cell survival, immune regulation, and bone development, providing insights into potential therapeutic targets for diseases including glioma, colon cancer, non - small cell lung cancer, and retinal degeneration [1,3,4,6,8].