EVA1B promotes non-small cell lung cancer progression through an LRG1-associated mechanism

Non-small cell lung cancer (NSCLC) remains a major cause of cancer-related mortality, mainly due to tumor growth and metastasis. This study investigated the biological role of Eva-1 homolog B (EVA1B) in NSCLC and its relationship with leucine-rich alpha-2-glycoprotein 1 (LRG1). Bioinformatic analysis showed subtype-specific expression patterns of EVA1B and LRG1 in NSCLC and suggested a potential functional association between them. In paired clinical samples, EVA1B expression was higher in tumor tissues than in matched paracancerous tissues, as shown by immunohistochemistry and Western blot analysis. EVA1B was also upregulated in A549 and H1299 cells compared with BEAS-2B cells. Functional assays showed that EVA1B knockdown inhibited NSCLC cell proliferation, migration, and invasion. These effects were accompanied by increased E-cadherin expression and decreased N-cadherin, Vimentin, and matrix metalloproteinase 11 expression, suggesting attenuation of the epithelial-mesenchymal transition-like phenotype. In vivo, EVA1B knockdown reduced xenograft tumor growth and lung metastatic burden. Mechanistically, co-immunoprecipitation suggested that EVA1B and LRG1 were present in the same immunoprecipitated protein complex. Together, these findings suggest that EVA1B contributes to NSCLC progression and may act, at least in part, through an LRG1-related mechanism.

The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05034-0.