Vcan, also known as extracellular matrix proteoglycan 2, is an extracellular matrix component. It is involved in multiple biological processes and signaling pathways. For instance, it may function through the PI3K/AKT1 signaling pathway [1]. Vcan is of great biological importance as it can regulate cell-cell and cell-matrix interactions, which are crucial for normal tissue development and function. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its function.

In a cardiac fibroblast-specific Vcan conditional knockout (CKO) mouse model using Col1a2-2A-CreER and Vcanfl/fl mouse strains, deletion of Vcan in cardiac fibroblasts decreased cardiomyocyte proliferation and impaired neonatal heart regeneration. This indicates that Vcan, which is upregulated after neonatal myocardial injury, promotes cardiomyocyte proliferation and is essential for neonatal heart regeneration [2].

In conclusion, Vcan plays a significant role in promoting cardiomyocyte proliferation and cardiac repair, as demonstrated by the CKO mouse model. In the context of cancer, it is involved in processes like epithelial-mesenchymal transition (EMT), anoikis resistance, and invasion, highlighting its importance in understanding and potentially treating cancer-related diseases [1,3].