Rescue experiments revealed that overexpressing BCL2L11 counteracted PVT1 knockdown-mediated restoration of the viability, repression of apoptosis and decrease of inflammatory cytokine production in CSE-induced 16HBE cells, indicating that PVT1 regulated COPD progression in vitro via the miR-30b-5p/BCL2L11 axis. This evidence concerns the gene PVT1 and chronic obstructive pulmonary disease.