This　study　aimed　to　investigate　the　correlation　of　C-X-C　chemokine　receptor　2　(CXCR2)　with　clinicopathological　characteristics　and　survival　in　non-small　cell　lung　cancer　(NSCLC)　patients　and　further　explore　its　effect　on　proliferation,　apoptosis,　invasion,　stemness,　chemosensitivity　as　well　as　JAK2/STAT3　pathway　in　NSCLC　cells.　The　expression　of　CXCR2　in　tumor　tissues　and　adjacent　tissues　from　340　NSCLC　patients　received　surgery　was　detected　by　immunohistochemistry.　CXCR2　overexpression　and　knockdown　were　constructed　through　plasmid　transfection　and　the　effect　of　CXCR2　dysregulation　on　cell　proliferation,　apoptosis,　invasion,　stemness,　chemosensitivity　as　well　as　its　regulatory　effect　on　JAK2/STAT　signaling　pathway　was　assessed　in　NCI-H1437　cells　and　NCI-H1299　cells.　CXCR2　expression　was　higher　in　tumor　tissues　than　that　in　paired　adjacent　tissues,　and　it　was　correlated　with　poor　pathological　differentiation,　greater　tumor　size,　lymph　node　metastasis,　higher　TNM　stage　and　poor　survival　in　NSCLC　patients.　In　vitro,　CXCR2　expression　was　increased　in　human　NSCLC　cell　lines　compared　with　human　normal　lung　bronchus　epithelial　cells.　CXCR2　promoted　cell　proliferation　and　invasion,　while　suppressed　cell　apoptosis　in　NCI-H1437/NCI-H1299　cells.　Additionally,　CXCR2　increased　CD133(+)　cell　rate　and　cell　sphere-forming　ability,　while　reduced　chemosensitivity　to　cisplatin　and　gemcitabine　in　NCI-H1437/NCI-H1299　cells.　Besides,　CXCR2　activated　the　JAK2/STAT3　signaling　pathway　in　NCI-H1437/NCI-H1299　cells.　In　conclusion,　the　clinical　implication　and　the　molecular　function　of　CXCR2　discovered　in　our　study　reveal　the　potential　of　CXCR2　as　a　future　target　for　disease　monitoring　and　treatment　of　NSCLC.