Itga2, also known as CD49b or VLA-2, is the alpha subunit of the transmembrane collagen receptor integrin alpha-2/beta-1. It is involved in cell adhesion, and its associated pathways may include those related to DNA damage response, immune regulation, and extracellular matrix-mediated cell-cell interactions. It plays an important role in various biological processes such as cell growth, invasion, and DNA repair, and is thus of great biological significance. Genetic models, like KO/CKO mouse models, can be valuable for studying its functions [1,5].

In pancreatic cancer, overexpression of Itga2 inhibits DNA repair by restraining the recruitment of DNA-PKcs to Ku70/80 heterodimer in the non-homologous end joining (NHEJ) pathway, conferring sensitivity to radiotherapy. It also affects immune regulation by influencing the expression of MET, PD-L1, CD4, and CD8, and induces STING expression by degrading DNMT1 [1,2,5]. In glioblastoma, Itga2 is a potential nanotherapeutic target as its antibody blockade impedes cell migration. In colorectal cancer, it enhances 5-fluorouracil resistance, and this can be overcome by selumetinib [3,4]. In esophageal squamous cell carcinoma, overexpression of Itga2 promotes tumor cell proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) via the FAK/AKT signaling pathway [6]. In intrahepatic cholangiocarcinoma, elevated Itga2 expression promotes collagen type I-induced clonogenic growth. In thyroid carcinoma, hypomethylation-mediated overexpression of Itga2 stimulates cell invasion and migration. In glioma, Itga2 promotes glioma stem cell (GSC) invasion and EMT by activating STAT3 phosphorylation [7,8,9].

In conclusion, Itga2 has diverse functions in multiple biological processes and disease conditions. Through model-based research, especially KO/CKO mouse models, it has been revealed that Itga2 is involved in DNA repair, immune regulation, cell growth, invasion, and migration in various cancers, providing potential therapeutic targets for these diseases.