Fbxo22, an F-box E3 ligase and a member of the F-box protein family, is involved in multiple biological processes. It is part of the SCF E3 ligase complex and plays a role in ubiquitin-dependent protein degradation, which is crucial for controlling various cellular processes such as cell cycle, transcriptional regulation, and apoptosis [2,3,4].

In leukemia, a hematopoietic cell-specific Fbxo22 knockout mouse model was established. Deletion of Fbxo22 in this model dramatically abrogated MLL-AF9-induced leukemogenesis and reduced leukemia stem cells after serial transplantations. Mechanistically, FBXO22 promotes MLL-rearranged AML progression by targeting BACH1 for degradation [1]. In hepatocellular carcinoma, knockdown of FBXO22 in vitro and in vivo inhibited cell proliferation, while overexpression promoted tumor formation. FBXO22 promotes tumor development by regulating the ubiquitination and degradation of p21 [2].

In conclusion, Fbxo22 is essential in the ubiquitin-mediated protein degradation pathway. The gene knockout models in mice have revealed its oncogenic roles in leukemia and hepatocellular carcinoma, highlighting its potential as a therapeutic target in these diseases. Understanding Fbxo22 function through such models can provide new strategies for cancer treatment.