Bgn, also known as biglycan, is an extracellular matrix proteoglycan. It can bind to transforming growth factor beta (TGF-β) to regulate its free concentration [5]. Bgn is involved in multiple biological processes, such as bone formation, tissue repair, and is related to signaling pathways like NF-κB, JAK2/STAT3 [1,2,6]. It has significance in various physiological and pathological conditions, including tumor progression, aortic stenosis, and osteoarthritis [1,2,4].

In gastric cancer, Bgn promotes tumor progression and the transformation of mesothelial cells into cancer-associated fibroblasts like cells (CAFLCs), and forms a BGN/FAP-STAT3 positive feedback loop with CAFLCs, facilitating peritoneal metastasis [1]. In aortic stenosis, Bgn is a new endogenous agonist of TLR3, and Bgn-/-mice are protected against aortic stenosis and display impaired bone formation, indicating its role in the BGN-TLR3-IFN axis in calcification of the aortic valve [2]. In colorectal cancer, down-regulation of Bgn expression in cancer-associated fibroblasts significantly reduces the migration and proliferation of CRC cells, and high infiltration of BGN + Fib is associated with poor prognosis [3].

In conclusion, Bgn is an important proteoglycan involved in multiple biological processes and diseases. Gene knockout mouse models, such as Bgn-/-mice, have revealed its role in tumor metastasis, aortic stenosis, and colorectal cancer progression, providing insights into disease mechanisms and potential therapeutic targets.