Lung　adenocarcinoma　(LUAD)　is　the　most　common　histological　subtype　of　lung　cancer,　characterized　by　a　high　incidence　in　late　stages,　high　mortality　rate,　and　poor　prognosis.　Src　Homology　2　Domain　Containing　Protein　5　(SH2D5)　is　a　mammalian-specific,　uncharacterized　scaffolding　protein,　and　its　role　in　LUAD　remains　unclear.　In　the　present　study,　we　investigated　the　function　and　potential　mechanisms　of　SH2D5　in　the　progression　of　LUAD.　We　found　aberrant　expression　of　SH2D5　in　LUAD　tissues　and　cells,　and　its　high　expression　is　closely　associated　with　poor　prognosis　in　LUAD　patients.　Through　loss-of-function　and　gain-of-function　experiments,　we　revealed　that　overexpression　of　SH2D5　promotes　the　proliferation　and　migration　abilities　of　lung　adenocarcinoma　cells.　Gene　set　enrichment　analysis　(GSEA)　revealed　that　SH2D5　positively　regulates　the　epithelial-mesenchymal　transition　(EMT)　process　in　lung　adenocarcinoma　cells.　Additionally,　we　found　that　regulating　the　expression　of　SH2D5　influenced　the　phosphorylation　levels　of　AKT,　and　the　rescue　experiments　with　AKT　pathway　activators/inhibitors　partially　reversed　the　tumor　progression　and　EMT　processes　induced　by　SH2D5.　In　summary,　our　study　demonstrated　that　SH2D5　promotes　the　migration　and　EMT　process　of　LUAD　cells　through　the　AKT　signaling　pathway,　suggesting　that　SH2D5　may　serve　as　a　crucial　potential　target　for　the　treatment　of　metastatic　LUAD.