Objective  To investigate the expression of dynein axonemal intermediate chain 1(DNAI1) in lung adenocarcinoma(LUAD) and its influence on invasive ability of lung adenocarcinoma.   Methods  Microarray gene chip analysis was used to screen different expression genes in lung adenocarcinoma(3 samples) and adjacent normal tissues(3 samples); Heatmap and volcano plot were performed demonstrate the mRNA expression and distribution after screening; DAVID database used for Gene Ontology(GO) and Kyoto Encyclopedia of Genes of Genomes(KEGG) analysis; STRING database and Cytoscape 3.6.1 software for protein-protein interaction (PPI) analysis and screening of Hub genes; Objective genes were selected based on the differential expression of each Hub gene in lung adenocarcinoma in DEGs and Ualcan database ; Real-time PCR and Western blotting were used to detect the expression of DNAI1 in BEAS-2B, H1299 and A549; observe the morphological changes after DNAI1 overexpression; Transwell invasion assay was used to detect the change of invasion ability of A549 cells after DNAI1 overexpression.   Results  The microarray result  showed that there were 86 up-regulated genes and 396 down-regulated genes; different genes were involved in the RNA polymerase Ⅱ promoter positive regulation of transcription, apoptosis process of negative regulation, protein binding, and other functions, widely distributed within the cell, and associated with the metabolic pathway, cancer and other signal pathways were closely related; DEGs database and Ualcan database showed that DNAI1 was the most downregulated among Hub genes in LUAD; the result  of Real-time PCR and Western blotting showed that DNAI1 had lower expression in H1299 and A549 compared with BEAS-2B; after DNAI1 overexpression, A549 cells became round and a few shed off; invasion assay showed that the invasion ability of A549 cells was significantly reduced.    Conclusion DNAI1 has a lower expression and inhibits the ability of invasion in LUAD, and this study can provide a potential molecular target and provide a theoretical basis for targeted therapy of LUAD.