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Abstract: Background chronic obstructive pulmonary disease (COPD) is a severe public health problem. cigarette smoke (CS) is a risk factor for COPD and lung cancer. The underlying molecular mechanisms of CS-induced malignant transformation of bronchial epithelial cells remain unclear. In this study, we describe a lung-on-a-chip to explore the possible mechanistic link between cigarette smoke extract (CSE)-associated COPD and lung cancer. Methods An in vitro lung-on-a-chip model was used to simulate pulmonary epithelial cells and vascular endothelial cells with CSE. The levels of IL-6 and TNF-α were tested as indicators of infammation using an enzyme-linked immune sorbent assay. Apical junction complex mRNA expression was detected with qRT-PCR as the index of epithelial-to-mesenchymal transition (EMT). The efects of CSE on the phosphorylation of signal transduction and transcriptional activator 3 (STAT3) were detected by Western blotting. Flow cytometry was performed to investigate the efects of this proto-oncogene on cell cycle distribution. Results Infammation caused by CSE was achieved in a lung-on-a-chip model with a mimetic movement. CSE exposure induced the degradation of intercellular connections and triggered the EMT process. CSE exposure also activated the phosphorylation of proto-oncogene STAT3, while these efects were inhibited with HJC0152. Conclusions CSE exposure in the lung-on-a-chip model caused activation of STAT3 in epithelial cells and endothelial cells. HJC0152, an inhibitor of activated STAT3, could be a potential treatment for CS-associated COPD and lung cancer.