The increased proliferation and migration of airway smooth muscle cells (ASMCs) are essential factors in the development of asthma. Long noncoding RNAs (lncRNAs) play key roles in the pathogenesis of various diseases, including asthma. A growing body of evidence indicates that lncRNA FTX regulates proliferation and migration in multiple cell types and the progression of various diseases. However, the role of FTX in asthma is still not yet fully understood. Therefore, we explored the role of FTX in the proliferation and migration of ASMCs stimulated by platelet-derived growth factor BB (PDGF-BB) in vitro, as well as the underlying molecular mechanisms. Here, it is demonstrated that the expression of FTX in ASMCs treated with PDGF-BB is significantly up-regulated, and FTX knockout effectively represses the proliferation and migration and promotes the apoptosis of ASMCs induced by PDGF-BB. Mechanistically, FTX can inhibit the proliferation and migration of ASMCs caused by PDGF-BB by targeting miR-590-5p, and FTX over-expression reverses the inhibitory effect. Furthermore, JAK2 is a direct target of the FTX/miR-590-5p signal axis, the over-expression of which reverses the inhibitory effect on the proliferation and migration and the apoptosis-inducing effect of miR-590-5p in ASMCs. Collectively, these results highlight the crucial regulatory role of the FTX/miR-590-5p/JAK2 axis in ASMC proliferation, migration, and apoptosis.