VIM and neoplasm: This process is characterized by a state with a less epithelial phenotype and a more mesenchymal phenotype, mainly manifested by downregulation of epithelial markers such as E-cadherin and claudin 1 (ZO-1) expression and induction of mesenchymal markers such as N-cadherin, fibronectin (FN), Vimentin, and zinc finger E-box binding protein 1 (ZEB1) elevation, ultimately leading to the weakening of intercellular adhesion and loss of cell polarity, which ultimately enhances tumor invasion and migration [10].