Barx1, a homeobox-containing gene, is expressed in various tissues during development, such as the mesenchymal cells of molar teeth and stomach in mice [3]. It has an instructive role in molar development, guiding undetermined ectomesenchymal cells in the jaws to follow a multicuspid tooth developmental pathway. In the presumptive stomach mesenchyme, it attenuates Wnt signalling to allow the differentiation of digestive tract endoderm into stomach epithelium. Genetic models, like gene knockout in mice, are valuable for studying its function.

In cancer research, loss-of-function studies have shown its significance. In NSCLC, loss of ZFP36 leads to BARX1 upregulation, promoting cell proliferation, migration, and invasion by transactivating master oncogenes [1]. In osteosarcoma, downregulating BARX1 suppresses cell proliferation and migration, while its overexpression has the opposite effect, and it acts by regulating HSPA6 expression [2]. In lung adenocarcinoma, BARX1 deficiency limits malignant phenotypes, and it represses FOXF1 expression and activates the Wnt/β-catenin signalling pathway to drive the disease [4].

In conclusion, Barx1 plays essential roles in development, especially in tooth and stomach development. In disease, particularly in multiple types of cancer, model-based research, including gene knockout studies, has revealed its role in promoting malignant phenotypes. Understanding Barx1 function can provide insights into disease pathogenesis and potential therapeutic targets in cancer.