Sox7, a member of the SOX (SRY-related HMG-box) family of transcription factors, plays crucial roles in multiple biological processes. It is involved in hematopoiesis, vasculogenesis, and cardiogenesis during embryonic development [2]. In the cardiovascular system, it is associated with pathways such as VEGF/Flk1 signaling, Wnt signaling, and the Notch pathway [3].

In mice, endothelial-specific loss of Sox7 function leads to cardiac ventricular defects similar to non-compaction cardiomyopathy, with abnormal coronary artery formation. This phenotype is due to disrupted transcriptional regulation of the Notch pathway and connexins 37 and 40, as well as depletion of a subset of Sox9/Gpc3-positive endocardial progenitor cells and an increase in erythro-myeloid cell lineages. Some Sox7-null endothelial cells transdifferentiate into hematopoietic lineages [1]. In addition, Sox7-overexpression in BCa cell lines inhibits the proliferative, migratory, and invasive capabilities of BCa, via the DNMT3B/CYGB axis [4].

In conclusion, Sox7 is essential for maintaining cardiac endothelial cell identity, which is crucial for ventricular compaction and coronary artery development. It also plays a tumor-suppressive role in various cancers like bladder cancer. The study of Sox7 using gene-knockout mouse models has provided valuable insights into its functions in heart development-related diseases and cancer [1,2,4].