In summary, our study demonstrates that, SphK1 acts as a downstream effector of IGF-1 and plays a critical role in IGF-1-induced EMT, migration and paclitaxel resistance of A549 cells, suggesting that SphK1 might be a promising target for the development of a more effective lung cancer therapy, and for the prevention of tumor metastases and drug resistance. This evidence concerns the gene IGF1 and lung carcinoma.