Itgb5-KO Mouse

Itgb5, encoding integrin β5 subunit, is crucial in cell adhesion and binding. It assorts with the αv subunit to form integrin αvβ5, and is involved in multiple signaling pathways like integrin signaling, which is essential for various biological processes such as cell-matrix interactions, cell migration, and tissue development [3].

In multiple cancers, Itgb5 shows oncogenic roles. In gastric cancer, knockdown of Itgb5 impairs cell metastasis both in vitro and in vivo, as Itgb5 promotes TGFBR2 endosomal recycling, facilitating epithelial-mesenchymal transition mediated by TGFβ signaling [1]. In pancreatic adenocarcinoma, knocking down Itgb5 increases cell sensitivity to radiation by influencing DNA damage repair and the MEK/ERK signaling pathway [2]. In hepatocellular carcinoma, Itgb5 confers sorafenib resistance through a positive feedback loop involving EPS15, EGFR, and CSNK1A1 [4]. In colorectal cancer, silencing Itgb5 inhibits cell proliferation, invasion, and migration by blocking the Wnt/β-catenin signaling pathway and epithelial-mesenchymal transition [5]. In addition, in piglets, disruption of Itgb5 in IPEC-J2 cell lines using CRISPR/Cas9 significantly reduces the adhesion of enterotoxigenic Escherichia coli F4ac to porcine intestinal epithelial cells, suggesting its role in ETEC F4ac-induced diarrhea [3].

In conclusion, Itgb5 is mainly involved in cell adhesion-related functions and plays important roles in multiple disease conditions, especially in promoting cancer metastasis and drug resistance. Studies using gene knockout or knockdown models in various organisms and cell lines have been crucial in revealing these functions, providing potential therapeutic targets for cancers and insights into other diseases like ETEC-induced diarrhea in piglets.