Cux2, or Cut-like homeobox 2 gene, encodes a transcription factor. It plays crucial roles in multiple biological processes such as neuronal development including proliferation, dendrite branching, and synapse formation [4,5,7]. It is also involved in limb development, regulating the positioning of forelimb buds [6]. Associated pathways include those related to histone modification, epithelial-mesenchymal transition, and various signaling cascades like PI3K-AKT-mTOR [3]. Genetic models, especially mouse models, have been valuable in studying Cux2's functions.

In cancer research, Cux2 has distinct roles. In breast cancer, its high expression promotes tumorigenesis and progression via the CUX2/KDM5B/SOX17 axis. Inhibition of Cux2 suppresses cell malignant phenotypes [1]. In gliomas, Cux2 has low expression, and its overexpression represses cell proliferation, migration, and invasion by enhancing ADCY1 transcription [2]. In papillary thyroid cancer, Cux2 functions as an oncogene, and its silencing inhibits cell proliferation, colony formation, migration, invasion, and induces apoptosis [3]. In epilepsy research, Cux2 deficiency in mouse models causes facilitation of excitatory synaptic transmission onto the hippocampus and increased seizure susceptibility to kainate [4].

In conclusion, Cux2 is a key regulator in neuronal and limb development. In disease areas, especially cancer and epilepsy, research using gene knockout (KO) or conditional knockout (CKO) mouse models has revealed its significant roles. Understanding Cux2's functions provides insights into the mechanisms of these biological processes and diseases, potentially offering new therapeutic targets.