By activating FOXM1, MELK significantly promoted the malignant phenotypes of ESCC cells, this conclusion was based on the following facts: (1) Ectopic expression of MELK promoted, while lentiviral shRNA mediated gene silencing diminished the expression of p-FOXM1 (T600) and its downstream targets including Cyclin B1, PLK1, Aurora B and Survivin both in vitro and in vivo; (2) Overexpression of FOXM1 diminished the inhibitory effect of MELK shRNAs on ESCC cell growth, migration and invasion. This evidence concerns the gene MELK and esophageal squamous cell carcinoma.