Nrp2, or Neuropilin-2, is a single-chain transmembrane glycoprotein. It acts as a co-receptor of VEGF and is involved in multiple biological processes [1]. It has been associated with pathways like Wnt/β-catenin, TGFβ1-related signaling, and is important in angiogenesis, cell apoptosis, and tumorigenesis [1,2,4]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its function.

In cancer research, Nrp2 has been shown to act as a tumor promoter. In oral squamous cell carcinoma (OSCC), knockdown of Nrp2 inhibited cell proliferation, migration, and invasion, and downregulated the Wnt/β-catenin pathway [1]. In bladder cancer, Nrp2 was linked to epithelial-to-mesenchymal transition (EMT) and chemoradioresistance, and in pancreatic neuroendocrine tumors (PNETs), blocking Nrp2 in vivo suppressed angiogenesis and tumor growth [2,4]. In atherosclerosis, Nrp2 knockdown in mice mitigated the development of atherosclerosis by regulating endothelial cell apoptosis [3].

In conclusion, Nrp2 is a crucial regulator in various biological processes and disease conditions. KO/CKO mouse models have revealed its role in promoting tumorigenesis in multiple cancers, contributing to atherosclerosis, and regulating angiogenesis. Understanding Nrp2's function provides potential therapeutic targets for treating cancer and atherosclerotic disorders.