Arid3b, a member of the AT-rich interaction domain (ARID) family of transcription factors, is evolutionarily conserved and involved in multiple biological processes. It is part of a transcription-activating complex with ARID3A and histone demethylase 4C (KDM4C), and is associated with pathways like LIN28-let-7, which is crucial for placental development [1]. It also plays roles in cell cycle regulation, chromatin remodeling, and is linked to processes such as cellular immortalization and epithelial-mesenchymal transition (EMT) [3].

Arid3b-deficient mouse embryos display cardiac abnormalities, including shortening of the poles, absence of myocardial differentiation, and altered atrioventricular canal patterning. This is due to a defect in the addition of second heart field progenitors to the heart, suggesting Arid3b is required for heart development by regulating progenitor motility and differentiation [4]. In hematopoiesis, bone marrow lacking Arid3b shows decreased common lymphoid progenitors (CLPs) and downstream B cell populations, indicating that B cell development requires Arid3b [6]. In ovarian cancer, overexpression of ARID3B in nude mice increases tumor burden, decreases survival, and boosts production of CD133+ (cancer stem cell marker) cells, enhancing paclitaxel resistance [5]. In gastric cancer, ARID3B over-expression suppresses cell proliferation, migration, and metastasis, and is an independent prognostic factor [2].

In summary, Arid3b is essential for multiple biological processes. Its deficiency in mouse models reveals its critical role in heart development, B-lymphocyte development, and its impact on cancer progression in ovarian and gastric cancers. Understanding Arid3b function through these models provides insights into congenital malformations and cancer biology, potentially guiding future therapeutic strategies.