Loss of SARI expression initiates epithelial-to-mesenchymal transition (EMT), which is visualized by repression of E-cadherin and up-regulation of vimentin in lung adenocarcinoma cell lines and in clinical lung adenocarcinoma specimens.

Vimentin expression predicts the occurrence of metastases in non small cell lung carcinomas.

Authors propose a model whereby vimentin promotes FAK stabilization through VAV2-mediated Rac1 activation. This model may explain why vimentin expressing metastatic lung cancer cells are more motile and invasive.

High vimentin expression is associated with invasion and metastasis of hypoxic non-small cell lung cancer.

Vimentin Regulates Invasiveness and Is a Poor Prognostic Marker in Non-small Cell lung cancer

Vimentin induced by exosomes is necessary for lung cancer to induce mesenchymal transition (EMT) in recipient bronchial epithelial cells (HBECs).

High vimentin expression is associated with Non Small-cell lung cancer.

VIM is downregulated and E-cad is upregulated in T1 stage non-small-cell lung cancer, suggesting that a mesenchymal-epithelial transition may take place in the early-stage of tumor development

Silencing of Vimentin in CNE2 cells leads to a decrease of microvessel density and VEGF, CD31, MMP2, and MMP9 expressions in pulmonary metastatic tumors.

These data show that vimentin is required for lung adenocarcinoma metastasis by maintaining heterotypic tumor cell-CAF interactions during collective invasion.

Mechanistic analyses revealed that FOXD1 expressed its oncogenic characteristics through activating Vimentin in non-small cell lung cancer cells.

Results find that VIM overexpression was significantly correlated with poor disease-free and overall survival of patients with lung adenocarcinoma. Vimentin is a key factor linking EMT and EZH2 in lung adenocarcinoma.

ATM modulates vimentin expression to facilitate IL-6-induced epithelial-mesenchymal transition and metastasis in lung cancer, indicating that ATM and vimentin might be potential therapeutic targets for inflammation-associated lung cancer metastasis.