Itgb3, encoding integrin subunit beta 3, is a cell adhesion molecule involved in cell movement [2]. It is associated with multiple signaling pathways including MAPK and VEGF, and plays crucial roles in various biological processes such as cell proliferation, migration, invasion, adhesion, and apoptosis [1,2]. Gene knockout models, like Itgb3 -/- mice, are valuable for studying its functions.

In osteosarcoma, Itgb3 promotes cell proliferation and cisplatin resistance via the MAPK and VEGF signaling pathways, and its knockout leads to decreased cell proliferation and migration due to increased apoptosis and slowed cell cycle progression [1].

In preeclampsia, Itgb3 expression is reduced in placental tissue, and in vitro experiments on HTR8/SVneo cells show that Itgb3 enhances trophoblast cell proliferation, migration, invasion, and adhesion while inhibiting apoptosis [2].

In lung adenocarcinoma, Itgb3 -enriched extracellular vesicles mediate the formation of an osteoclastic pre-metastatic niche to promote bone metastasis [4].

In Itgb3 -/- mice, platelet functions are impaired, accompanied by decreased platelet count, microcytic hypochromic anemia, and splenomegaly, but these mice have unique characteristics different from human patients with Glanzmann thrombasthenia [3].

In conclusion, Itgb3 is essential for cell adhesion-related functions and is involved in multiple disease conditions. Gene knockout mouse models have provided insights into its role in osteosarcoma, preeclampsia, lung adenocarcinoma bone metastasis, and platelet-related functions, helping to better understand the underlying molecular mechanisms and potentially identify new therapeutic targets.