provides support that E-cadherin induction by WNT/beta-catenin signaling is an evolutionarily conserved pathway operative in lung cancer cells and that loss of expression may be important in lung cancer development or progression

E-cadherin and p16INK4a are commonly methylated in non-small cell lung cancer

Loss of expression of E-cadherin and beta-catenin may play an important role in the progression of pulmonary adenocarcinoma

Serum levels may be a prognostic biological marker innonsmall cell lung cancer.

Reduced E-cadherin expression is related to a poor prognosis through hematogenous metastasis in pulmonary adenocarcinoma.

Roles of E-cadherin and beta-catenin complexes in signet ring cell carcinoma of the lung differ from their roles in gastric or colorectal cancers.

-160A of the E-cadherin gene is emerging as a low-penetrance tumor susceptibility allele for the development of gastric, lung, prostate, and urothelial cancers.

expression of S100A4 protein and loss of E-cadherin protein expression are significantly associated with tumor progression in non-small cell lung cancer.

E-cad, CD44v6 and PCNA play important roles in invasion and metastasis of non-small cell lung cancer (NSCLC).

promoter-hypermethylation of E-cad is significantly associated with its defective expression and tumor differentiation in non-small cell lung cancer

Core-fucosylated E-cadherin regulated nuclear beta-catenin accumulation in lung cancer cells.

recruitment of E-cadherin expression by Connexin 43 and inhibits the malignant behaviour of lung cancer cells

In squamous cell lung cancer or lung adenocarcinomas, the abnormal cytoplasmic expression of p120ctn isoform 1 always correlates to the abnormal expression of E-cadherin.

e-cadherin is a prognostic factor for non-small cell lung cancer

Reduced E-cadherin or beta-catenin negative expression relates to dedifferentiation and progression of nonsmall cell lung cancer

Overexpressions of nuclear E-cadherin is associated with non-small cell lung cancer.

In lung carcinomas dysadherin expression seems to reflect tumour aggressiveness and may be considered a positive marker of poor prognosis when considered alone or/and in combination with down-regulation of E-cadherin.

Brain metastases originating from lung adenocarcinoma and small cell lung cancer were significantly associated to E-cadherin genetic changes.

Fyn, a member of Src family tyrosine kinases, plays a critical role in mediating TGF-beta1-induced down-regulation of E-cadherin in human A549 lung cancer cells.

Data suggest that pulmonary metastasis is corrected with levels of Geminin, cleaved caspase-3, CD44, E-cadherin, epidermal growth factor receptor, and CD204 in cancer cells within permeated lymphatic vessels.

Investigated the expression of RKIP and E-cadherin in lung squamous cell carcinoma tissue. The rates of positive RKIP and E-cadherin mRNA expression were significantly lower in lung squamous cell carcinoma than in the surrounding normal tissues.

Decreased E-cadherin expression was associated with poor survival in patients with non-small cell lung cancer, especially among Asians. [Meta-analysis]

findings suggest that miR-23a regulates TGF-beta-induced epithelial-mesenchymal transition by targeting E-cadherin in lung cancer cells

These results provide strong evidence that the methylation status of E-cadherin gene contributes to a reduction in the expression of E-cadherin mRNA, and may play a role in the development and progression of non-small cell lung cancer.

Ezrin, E-cadherin and CD44V6 play an important role in the regulation of growth and meastasis of lung cancer.

The aim of this study is to evaluate the role of p130cas, E-cadherin, and beta-catenin expression in patients with non-small cell lung cancer.

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.

Key roles of ZEB1 and E-cadherin in the oncogenesis and invasiveness of lung squamous cell carcinoma.

The low expression of CD82/KAI1 and E-cadherin was closely related to the invasion, progression and metastasis of non-small cell lung cancer.

Decreased levels of E-cadherin is associated with lung cancer.

Data indicate that TIMP-2 promotes an anti-tumoral transcriptional profile in lung cancer including upregulation of E-cadherin.

Loss of E-cadherin expression is associated with poor response to epidermal growth factor receptor-tyrosine kinase inhibitor treatment in lung cancer.

Cx43 and E-cadherin are reduced with non-small cell lung cancer progression, and might be important biomarkers for judging the metastasis and prognosis.

methylation of E-cadherin promoter is associated with risk of lung cancer

Suppression of CDH1 transcription is associated with the development and progression of non-small-cell lung cancer.

Loss of E-cadherin is mediated through inhibition of mTORC1 in lung cancer cells.

Studies indicate that hypermethylation frequencies in lung cancer (LC) tissues were significantly higher than those in normal control tissues

Btbd7 contributes to reduced expression of E-cadherin and may be a promising cancer marker in non-small cell lung cancer.

Octamer-binding protein 4 affects the cell biology and phenotypic transition of lung cancer cells involving beta-catenin/E-cadherin complex degradation

The results from the current study indicate that the hypermethylation frequency of E-cadherin in NSCLC is strongly associated withnon-small cell lung carcinoma incidence and it may be an early event in carcinogenesis

ABCG2 localizes to the nucleus and modulates CDH1 expression in lung cancer cells

E-cadherin expression was associated with EGFR mutation status and patient prognosis in lung adenocarcinoma patients

In non-small cell lung cancer patients, the loss expression of beta-arrestin1 was frequently observed, and beta-arrestin1 expression was significantly correlated with the smoking index and E-cadherin expression, which all indicated beta-arrestin1's significant clinicopathologic role

Evaluation of FoxC2 expression, alone or in combination with E-cadherin expression, may help to stratify non-small cell lung cancer patients for risk of disease progression, pointing to this EMT regulator as a potential prognostic marker

EZH2 is recruited to the E-cadherin promoter by the long non-coding RNA, MALAT-1 (metastasis associated in lung adenocarcinoma transcript 1), where it represses E-cadherin expression

cancer stem cells amount in human lung adenocarcinoma cell line A549 depends on E-cadherin expression.

Thrombomodulin up-regulated E-cadherin but down-regulated N-cadherin expression, resulting in reversal of epithelial-mesenchymal transition (EMT) in the lung cancer cells.

studies indicate Bit1 is an inhibitor of EMT and metastasis in lung cancer and hence can serve as a molecular target in curbing lung cancer aggressiveness

Low expression of CDH1 is associated with invasion in non-small cell lung cancer.

Study shows that the protein level of E-CAD is indirectly regulated by MIR-193a in non-small cell lung cancers through downregulation of WT1.

E-cadherin expression was increased by transfection of p300 small interfering RNA in a dose-dependent manner.. There was a correlation between Snail and p300 expressions in lung cancer. Moreover, p300 acetylates Snail both in vivo and in vitro, and K187 may be involved in this modification.

Low CDH1 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

our data suggest that miR-1285-5p functions as a tumor promoter in the development of non-small-cell lung carcinoma by targeting Smad4 and CDH1, indicating a novel therapeutic strategy for non-small-cell lung carcinoma patients.

FDG uptake on PET was associated with negative E-cadherin expression in patients with lung adenocarcinoma.

reduction of Alex3 correlates with the development of non-small cell lung cancer and predicts adverse clinical outcome of non-small cell lung cancer patients. The effect of Alex3 on inhibiting invasion and migration may attribute to upregulation of E-cadherin expression through AKT-Slug pathway inactivation.

CDH1 single-nucleotide polymorphisms role in susceptibility to non-small cell lung cancer

In conditioned media of PIBF-deficient JEG-3 cells, primary lung and ovarian cancer cells MMP9 activity was reduced. PIBF silencing resulted in increased E-cadherin expression, suggesting that by down regulating E-cadherin expression, PIBF might interfere with the cell-cell adhesion mechanisms and by increasing MMP activity induced extracellular matrix degradation, facilitates the invasion of tumor cells.

TGF-beta1 induced epithelial-mesenchymal transition in non-small cell lung cancer cells by upregulating miR-9 and downregulating miR-9's target, E-cadherin.

CDH1 variants are significantly reverse associated with mutation of EGFR tyrosine kinase;CDH1 variants might contribute to pathological development in lung adenocarcinoma

The frequency of E-cadherin promoter hypermethylation in CT is significantly higher than in AC, indicating that promoter hypermethylation of E-cadherin plays an important role in non-small cell lung cancer carcinogenesis.

Investigated the role of Wnt11 in neuroendocrine (NE) differentiation, cell proliferation, and epithelial-to-mesenchymal transition in small-cell lung cancer (SCLC). Ascl1 plays an important role in regulating the Wnt signaling pathway and is one of the driver molecules of Wnt11 in SCLC. Wnt11 controlled NE differentiation, cell proliferation, and E-cadherin expression under the regulation of Ascl1 in SCLC cell lines.

Long non-coding RNA H19 is responsible for the progression of lung adenocarcinoma by mediating methylation-dependent repression of CDH1 promoter.

TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin.

Disruption in E-cadherin expression is associated with metastatic progression in lung cancer

activation of Wnt/beta-catenin signaling can combine with other oncogenic pathways in lung epithelium to produce a more aggressive tumor phenotype by imposing an embryonic distal progenitor phenotype and by decreasing E-cadherin expression

Study using metastatic murine mammary carcinoma cell line 4T1 shows that in sparsely plated 4T1 cells, E-cadherin levels are moderately reduced (~50%), leading to the development of collective migration. Knocking down E-cadherin blocked tether formation in these cells, leading to enhancement of migration rate and, at the same time, to suppression of lung metastases formation in murine mammary carcinoma model.