The results demonstrate that ZEB-1 directly inhibits SEMA3F expression in lung cancer cells.

*Inhibiting ZEB1 function may be an attractive target for non-small cell lung cancer therapeutic development.

ZEB1 and ZEB2 are key regulators of the The epithelial to mesenchymal transition (EMT) process in non-small cell lung cancer.

Data suggest that knockdown of ZEB-1 expression by lentivirus-delivered siRNA may provide a novel therapeutic target for the treatment of lung cancer.

Metastatic adenocarcinomas show a higher expression of zeb1 and twist than primary lung tumors, confirming previous findings and highlighting their significance in the metastatic process.

Overexpression of the ZEB1 gene is possibly associated with the occurrence, development, invasion of lung squamous cell carcinoma.

ZEB1 sensitizes lung adenocarcinoma cells to metastasis suppression by PI3K-targeted therapy

miR-144 promotes the apoptosis of lung cancer cells, and inhibits the proliferation, invasion and migration of lung cancer by regulating ZEB1 gene.

identified Zinc finger E-box-binding homeobox 1 (ZEB1) bond to FBP1 promoter to enhance DNA methylation in lung cancer cells. Our findings indicate that the down-regulation of FBP1 is a critical oncogenic event in lung cancer progression

miR-200b and ZEB1 might have roles in sensitivity to nintedanib in non-small cell lung cancer cells

miR-455 directly binds to 3'UTR of ZEB1 and suppresses the endogenous level of ZEB1 protein expression. overexpression of ZEB1 reverses miR-455-suppressed malignant phenotype of NSCLC cells. upregulation of ZEB1 expression is inversely associated with miR-455 expression in NSCLC tissues. Taken together, miR-455 as an anti-oncogene in non-small cell lung cancer through up-regulation of ZEB1

ZEB1-induced epithelial-to-mesenchymal transition and associated molecular changes in ESRP1 and CD44 contribute to early pathogenesis and metastatic potential in established lung cancer

Increased collagen deposition in metastatic tumor tissues as a direct consequence of amplified collagen gene expression in ZEB1-activated mesenchymal lung cancer cells.

The Thymidylate synthase (TS)-ZEB1 association was confirmed in clinical specimens from lung tumours and in a genetic mouse model of pancreatic cancer with ZEB1 deletion. Interestingly, TS itself appeared to have a regulatory role in epithelial-to-mesenchymal in cancer cells, as TS knockdown could directly reduce the EMT phenotype, the migratory ability of cells, the expression of stem-like markers, and chemoresistance.

ZEB1-AS1/miR-409-3p/ZEB1 constitutes a positive feedback loop to promote the tumorigenesis of non-small cell lung cancer

The overexpression of ZEB1 resulted in an increase in the proliferation activity and a significant decrease in the apoptosis and knockdown of ZEB1 reduced on the Invasion Ability of non-small cell lung cancer cells.

MAPK signaling dependency in epithelial lung cancer cells is due to the scaffold protein interleukin-17 receptor D (IL17RD), which is directly repressed by ZEB1.

LncRNA TTN-AS1 drives invasion and migration of lung adenocarcinoma cells via modulation of miR-4677-3p/ZEB1 axis.

High ZEB1 expression is associated with Non-Small Cell lung cancers.

Study found that ZEB1 was highly expressed in lung adenocarcinoma (LUAD) and there was a strong positive correlation between circ-TSPAN4 and ZEB1 expression in LUAD tissues. circ-TSPAN4 can upregulate ZEB1 expression via sponging and inhibiting miR-665 in LUAD.

Effect of CUL4A on the metastatic potential of lung adenocarcinoma to the bone.

this work suggests that tumor cell-derived ANGPTL2 accelerates activities associated with glycolytic metabolism in lung cancer cells by activating TGF-beta-ZEB1-GLUT3 signaling.

ZEB1-activated LINC01123 accelerates the malignancy in lung adenocarcinoma through NOTCH signaling pathway.

PARP-1 induces EMT in non-small cell lung carcinoma cells via modulating the transcription factors Smad4, p65 and ZEB1.

Low PRRX1 expression and high ZEB1 expression are significantly correlated with epithelial-mesenchymal transition and tumor angiogenesis in non-small cell lung cancer.

PD-L1 expression Status Predicting Survival in pulmonary Pleomorphic Carcinoma.

Kras/Tp53-mutant lung adenocarcinoma develops metastatic disease due to high expression of ZEB1

Ras induction of ZEB1 is required for tumour initiation in a lung adenocarcinoma model via Pten repression. A lower threshold of ZEB1 is sufficient for cancer initiation, whereas further induction is necessary for tumour metastasis.