MYBL2, also known as B-MYB, is a transcription factor of the MYB transcription factor family. It is essential in regulating vital cellular processes such as cell proliferation, differentiation, DNA repair, and cell cycle progression. It also plays a role in cell survival [2]. Dysregulation of these processes is associated with cancer development, making MYBL2 a gene of significant interest in cancer research. Genetically engineered mouse models can be valuable tools for studying MYBL2's functions.

In various cancers, MYBL2 shows oncogenic properties. In bladder cancer, MYBL2 deficiency suppressed cell proliferation and migration in vitro and in vivo, while overexpression had the opposite effect. MYBL2 could bind to and transactivate the promoter of CDCA3, promoting the malignant phenotype of bladder cancer cells [1]. In prostate cancer, genetic inhibition of Mybl2 in murine prostate cancer cell lines representing phenotypic plasticity decreased in vivo growth, cell fitness, and repressed gene expression signatures related to pluripotency and stemness [3]. In ovarian cancer, tumor-derived MYBL2 indicated poor prognosis, and its inhibition could reprogram the tumor microenvironment and reduce anti-PD-1 resistance [4].

In conclusion, MYBL2 is a central regulator of cell-related processes. Through model-based research, especially gene knockout (KO) or conditional knockout (CKO) mouse models, its role in promoting cancer progression in multiple cancer types has been revealed. These findings contribute to understanding the mechanisms of cancer development and offer potential therapeutic targets for treating related diseases.