Objective：To investigate the effect of stanniocalcin（STC1） on epithelial-mesenchymal transition（EMT） in chronic obstructive pulmonary disease（COPD）and the expression in bronchial epithelial cells. Methods：Western blot and immunofluorescence were used to examine EMT associated biomarkers including E-cadherin and alpha smooth muscle actin（α-SMA）. The STC1 mRNA and protein levels stimulated by cigarette smoke extract（CSE） in human bronchial epithelial（16HBE）cells were analyzed by real-time polymerase chain reaction（RT-PCR）and Western blot. Results：TGF-β induced EMT of 16HBE cells where the cell morphology changed from a typical multilateral paving stone-like appearance to a mesenchymal-like fusiform appearance along with the decreased expression of epithelium biomarker E-cadherin and the increased expression of mesenchymal cell markers α-SMA. rhSTC1 significantly inhibited the EMT changes mentioned above. The expression of STC1 was increased by CSE in a concentration-dependent manner in 16HBE cells. And this effect was inhibited by NF-κB inhibitor JSH23. Conclusion：STC1 was a protective factor to inhibit EMT during the development of COPD. CSE may stimulate bronchial epithelial cells，and increase the expression of STC1 through NF-κB signal，which may be the main source.