In lung cancer tissues, CCL2 secreted by TAMs promotes EMT through a dual regulatory mechanism: on one hand, it significantly downregulates the expression of the epithelial marker E-cadherin, while on the other, it simultaneously upregulates the expression levels of the mesenchymal marker vimentin, as well as matrix metalloproteinases MMP-2 and MMP-9, thereby enhancing the invasion and migration capabilities of NSCLC cells (87). This evidence concerns the gene VIM and lung cancer.