Background:　Lung　adenocarcinoma　(LUAD)　is　the　major　subtype　of　lung　cancer　and　the　most　lethal　malignant　disease　worldwide.　However,　the　molecular　mechanisms　underlying　LUAD　are　not　fully　understood.　Methods:　Four　datasets　(GSE118370,　GSE85841,　GSE43458　and　GSE32863)　were　obtained　from　the　gene　expression　omnibus　(GEO).　Identification　of　differentially　expressed　genes　(DEGs)　and　functional　enrichment　analysis　were　performed　using　the　limma　and　clusterProfiler　packages,　respectively.　A　protein-protein　interaction　(PPI)　network　was　constructed　via　Search　Tool　for　the　Retrieval　of　Interacting　Genes　(STRING)　database,　and　the　module　analysis　was　performed　by　Cytoscape.　Then,　overall　survival　analysis　was　performed　using　the　Kaplan-Meier　curve,　and　prognostic　candidate　biomarkers　were　further　analyzed　using　the　Oncomine　database.　Results:　Totally,　349　DEGs　were　identified,　including　275　downregulated　and　74　upregulated　genes　which　were　significantly　enriched　in　the　biological　process　of　extracellular　structure　organization,　leukocyte　migration　and　response　to　peptide.　The　mainly　enriched　pathways　were　complement　and　coagulation　cascades,　malaria　and　prion　diseases.　By　extracting　key　modules　from　the　PPI　network,　11　hub　genes　were　screened　out.　Survival　analysis　showed　that　except　VSIG4,　other　hub　genes　may　be　involved　in　the　development　of　LUAD,　in　which　MYH10,　METTL7A,　FCER1G　and　TMOD1　have　not　been　reported　previously　to　correlated　with　LUAD.　Briefly,　novel　hub　genes　identified　in　this　study　will　help　to　deepen　our　understanding　of　the　molecular　mechanisms　of　LUAD　carcinogenesis　and　progression,　and　to　discover　candidate　targets　for　early　detection　and　treatment　of　LUAD.