Itgb5, or integrin β5, is a key component of integrin proteins, which play essential roles in cell adhesion, migration, and signaling. Integrins are involved in numerous cellular processes and pathways, such as cell-matrix interactions, focal adhesion, and the regulation of various signaling cascades like the TGF-β, Wnt, and MAPK pathways. Itgb5 is crucial for normal physiological functions and its dysregulation is associated with various diseases [1,4,6].

In cancer research, Itgb5 has been shown to promote metastasis in gastric cancer. Knockdown of Itgb5 impairs gastric cancer cell metastasis both in vitro and in vivo. It acts as a scaffold, interacting with TGFBR2 and SNX17 to facilitate TGFBR2 endosomal recycling, enhancing TGF-β-mediated epithelial-mesenchymal transition and metastasis [1]. In pancreatic adenocarcinoma, knockdown of Itgb5 increases cell sensitivity to radiation by promoting 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 [6].

In conclusion, Itgb5 is essential for normal cell-matrix interactions and signal transduction. Through gene-knockout or knockdown models in cancer research, it has been revealed that Itgb5 plays a significant role in promoting cancer metastasis, resistance to therapy, and cancer cell growth. Understanding the functions of Itgb5 provides potential therapeutic targets for treating various cancers. Additionally, Itgb5 may be involved in other diseases such as osteoarthritis where it shows diagnostic potential [3], and in the context of Escherichia coli F4ac-induced diarrhea in piglets [5].