The present study suggested that APS can reduce the expression of S1PR1 and downstream molecules STAT3 and p-STAT3 and inhibit the accumulation of myeloid-derived suppressor cells in the premetastatic niche of the lung via the S1PR1/STAT3 pathway, thus indicating that APS may be considered as a potentially effective strategy for the treatment of patients with lung cancer. This evidence concerns the gene S1PR1 and lung carcinoma.