PRMT6 and chronic obstructive pulmonary disease: In this study, we identified that (i) PRMT6 protein decreased in COPD; (ii) cigarette smoke extract decreased the unstable protein PRMT6 in epithelial cells; (iii) FBXW17 interacted with PRMT6 and specifically mediated the proteasomal degradation of PRMT6 protein in the nucleus; (iv) inhibition of the proteasome pathway and knockdown of FBXW17 partly blocked CSE-induced PRMT6 protein reduction; and (v) FBXW17/PRMT6 signaling was involved in CSE-induced lung epithelial inflammation and apoptosis.