POU6F1, a member of the POU family of transcription factors, plays diverse roles in biological processes. It is involved in regulating gene expression through binding to specific DNA sites, containing TAAT motifs [6]. POU6F1 is associated with multiple pathways, such as the HIF1A signaling pathway in lung adenocarcinoma (LUAD), and is crucial for processes like cell differentiation, plasticity in the adult brain, and nerve regeneration.

In LUAD, POU6F1 is downregulated, and its low expression predicts unfavorable prognosis. It inhibits the growth and invasion of LUAD cells by binding and stabilizing RORA, which transcriptionally inhibits HIF1A and alters the expression of related genes [1]. In gastric cancer, POU6F1 promotes ferroptosis by increasing lncRNA-CASC2 transcription, which regulates the SOCS2/SLC7A11 signaling [2].

In the adult mouse olfactory bulb, loss of POU6f1 in CRHR1+ neurons reduces dendritic complexity and synaptic connectivity, highlighting its role in circuit plasticity [3]. In sciatic nerve regeneration, overexpression of POU6F1 in transgenic Schwann cells promotes their proliferation, anti-apoptosis, and migration, enhancing axonal regeneration and functional motor recovery [4].

In mouse pre-implantation development, the degradation of Pou6f1 by DIS3 is necessary for proper cell differentiation, as Pou6f1 represses the transcription of Nanog and Cdx2 when not degraded [5].

In summary, POU6F1 is essential for various biological functions, including cell growth regulation in cancer, ferroptosis in gastric cancer, circuit plasticity in the brain, and nerve regeneration. Gene-targeted mouse models, like the Dis3 knockout affecting Pou6f1 levels, have provided valuable insights into its role in pre-implantation development. Understanding POU6F1 can potentially offer new therapeutic targets for diseases such as LUAD and gastric cancer, and further our knowledge of neural development and nerve repair.