Cdh2, also known as N-cadherin, belongs to the classic cadherin family of Ca2+-dependent cell adhesion molecules. It plays a dual role in cell adhesion and β-catenin signaling, being crucial for numerous biological processes. During CNS development, it is involved in maintaining neuroepithelial integrity, neural tube closure, progenitor cell regulation, neural precursor migration, axon guidance, and synaptic development [3]. It also acts as a regulator of stem cell fate decisions [4].

In acute leukaemia, targeting Cdh2 within the malignant bone marrow microenvironment shows potential as a therapeutic approach, as it may help overcome treatment resistance and relapse [1]. In idiopathic pulmonary fibrosis, Cdh2, along with CALD1 and POSTN, is upregulated in TGF-β1-treated fibroblasts and IPF lung tissue samples. Knockdown of Cdh2 attenuates the expression of fibrotic markers, indicating its role in pulmonary fibrosis [2]. In glioblastoma, N-cadherin (Cdh2) upregulation mediates adaptive radioresistance, and its knockout in radioresistant glioma stem cells reverts the acquired phenotypes [5].

In summary, Cdh2 is essential for cell adhesion, signaling, and various developmental processes. Research using gene-targeted mouse models, such as knockout or knockdown in relevant cell types, has revealed its significant roles in diseases like acute leukaemia, idiopathic pulmonary fibrosis, and glioblastoma, providing potential therapeutic targets for these conditions.