Integrin β4 Regulates Cell Migration of Lung Adenocarcinoma Through FAK Signaling

• Published in: Molecular biotechnology 2024-02
• Main Authors: Zhang, Shusen, Liu, Chengyu, Liu, Dengxiang, Ning, Xuecong, Li, Hui, Zhang, Xiaochong, Lu, Yuanyuan, Zhang, Ping, Chen, Shubo, Cai, Zhigang
• Format: Article
• Language: English
• ISSN: 1073-6085; 1559-0305
• DOI: 10.1007/s12033-024-01061-5

The role of the integrin family in malignancy has received increasing attention. Many studies have confirmed that ITGB4 could activate multiple signal pathways and promote cell migration in various cancers. However, the regulatory role of integrin β4 (ITGB4) in lung adenocarcinoma (LUAD) is still unclear. Examination of the expression or survival analysis of ITGB4 in cells, pathological samples, and bioinformatics lung adenocarcinoma databases showed ITGB4 was highly expressed in LUAD and significantly associated with poor prognosis. Small interfering RNA and plasmids were performed to investigate the effect of changes in ITGB4 expression on lung adenocarcinoma. Focal adhesion kinase (FAK) inhibitor defactinib was used to further explore the molecular mechanism of ITGB4. The results showed depletion of ITGB4 inhibited migration and activation of FAK signaling pathways in lung adenocarcinoma cells. Moreover, increased ITGB4 expression activated FAK signaling and promoted cell migration, which can be reversed by defactinib. In addition, ITGB4 could interact with FAK in lung adenocarcinoma cells. ITGB4 may promote cell migration of lung adenocarcinoma through FAK signaling pathway and has the potential to be a biomarker for lung adenocarcinoma.