MELK and neoplasm: Additionally, MELK depletion also greatly downregulated the expression of mesenchymal markers such as N-cadherin, Vimentin and Snail, but upregulated epithelial marker E-cadherin expression, suggesting targeting MELK suppressed the process of GC cell epithelial–mesenchymal transition (EMT), which is an important step for the initiation of tumor metastasis (17).