Vsig2, or V-set and immunoglobulin domain containing 2, belongs to the immunoglobulin superfamily (IgSF) and functions as a coinhibitory molecule, mediating immune evasion of tumors [1]. It has been associated with multiple biological processes and disease-related pathways, including those involved in cancer progression, immune response, and potentially cardiovascular health [1,2,3]. Genetic models such as knockout (KO) or conditional knockout (CKO) mouse models could potentially be valuable in further exploring its function.

In pancreatic ductal adenocarcinoma (PDAC), VSIG2 was highly expressed in tissues and cells. Overexpression of VSIG2 facilitated the proliferation, invasion, and migration of PDAC cells, while its inhibition had opposite effects. Mechanistically, VSIG2 bound to LAMTOR2 and mTOR, enhancing their interaction and leading to elevated mTOR phosphorylation and activation of downstream molecules [1]. In colon cancer, VSIG2 was identified as a key candidate gene through weighted gene co-expression network analysis. Its encoded protein was mainly expressed in immune cells, and its expression was positively correlated with immune infiltration, suggesting it plays a role in immune invasion and antigen presentation in colon adenocarcinoma (COAD) [2].

In conclusion, VSIG2 is a gene with significant implications in cancer-related biological processes. The findings from studies related to PDAC and colon cancer highlight its potential as a biomarker for diagnosis and prognosis, as well as a novel therapeutic target. Research on VSIG2 using gene knockout or conditional knockout mouse models could further elucidate its role in disease mechanisms, potentially leading to new strategies for disease treatment and prevention [1,2].