The impact of BTK knockdown on lung adenocarcinoma growth and immune response

Abstract This study explores the molecular role of the BTK gene in lung adenocarcinoma (LUAD) progression and patient prognosis. Using a radiomics model based on BTK expression and PET‐CT data analyzed through DeeplabV3, alongside transcriptomic and clinical data from TCGA, we established a strong predictive relationship between BTK levels and LUAD outcomes. Our findings demonstrate that low BTK expression is linked to poorer prognoses. Experimental models, including cell lines and in vivo mouse studies, revealed that BTK deficiency leads to increased LUAD cell proliferation, invasion, and metastasis. Furthermore, in vivo models indicated that BTK knockdown results in enhanced tumor growth and diminished CD8+ T cell activity. These results suggest that BTK plays a crucial role in modulating LUAD progression and the tumor immune environment, highlighting its potential as a therapeutic target.