Genetic polymorphisms in the EZH2 gene is associated with lung cancer.

study finds EZH2 to be highly overexpressed in lung and other cancers, and show that EZH2 is integral to proliferation in cancer cells

EZH2 promotes progression and invasion of nonsmall cell lung cancer (NSCLC), and its expression is a novel prognostic biomarker in NSCLC.

miR-26a expression inhibited the expression of enhancer of zeste homolog 2 and transactivated downstream target genes, which suggests that EZH2 is a potential target of miR-26a; miR-26a plays an important role as an anti-oncogene in the molecular mechanism of lung cancer

EZH2 contributes to the progression of lung adenocarcinoma

EZH2 may play an important role in the progression and metastasis of lung cancer

EZH2 mRNA levels may serve as a prognostic predictor for patients with non-small cell lung cancer.

findings present evidence for the role of EZH2 in the regulation of cell cycle and apoptosis, providing a biological mechanism to explain the tumorigenicity of EZH2 in small-cell lung cancers

Genomic deregulation of the E2F/Rb pathway leads to activation of the oncogene EZH2 in small cell lung cancer.

In lung, EZH2 expression is involved in early pathogenesis of squamous cell carcinomas.

EZH2 depletion decreases the malignant potential of lung adenocarcinoma and sensitivity of the cells to both platinum-based and VEGFR-2-targeted therapy.

We for the first time proposed the role interleukin-1beta-mir-101-EZH2 axes in the particle-induced lung cancer

EZH2 promotes lung cancer progression via the VEGF-A/AKT signaling pathway.

High DNA methylation in small cell lung cancer defines distinct disease subtypes and correlates with high expression of EZH2.

High EZH2 expression is associated with cisplatin-resistance of non-small cell lung and gastric cancer.

EZH2 and Lat1 expression are co-regulated in models of cancer cell differentiation and co-expression is observed at the invasive front of human lung tumors.

Posttranscriptional silencing of MALAT1 by miR-217 provides a link, through EZH2, between ncRNAs and the EMT and establishes a mechanism for cigarette smoke extract-induced lung carcinogenesis.

EZH2 overexpression was associated with poor overall survival in lung cancer, this effect appears also significant when the analysis is restricted in Asian population, lung AC and stage I patients, but not among Caucasians.

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

Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.

EZH2 directly binds to the Puma promoter thus epigenetically repressing PUMA expression in non-small cell lung cancer cells.

Results suggest that long noncoding RNA FOXF1-AS1 might regulate epithelial-mesenchymal transition (EMT), stemness and metastasis of non-small cell lung cancer (NSCLC) cells via EZH2, indicating it as a therapeutic target for future treatment of NSCLC.

Transwell invasion assay, wound healing assay and flow cytometry results showed that the inhibition of EZH2 or the up-regulation of miR-101-3p inhibited the viability, migration, invasion and cell cycle but promoted cell apoptosis of lung squamous cell carcinoma.

Meta-analysis: EZH2 expression is significantly correlated with aggressive tumor behavior and poor prognosis in non-small cell lung cancer.

Results show that EZH2 expression was significantly higher in lung adenocarcinoma (LA) and that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression.

Confirmation of an oncogenic role for LINC00319 in clinical specimens and cellular experiments, showing the potential LINC00319/miR-450b-5p/EZH2 pathway in lung adenocarcinoma tumorigenesis.

AFAP1-AS1 epigenetically silences p21 transcription by binding to EZH2 thus promoting non-small cell lung cancer cell growth.

Enhancer of zeste homolog 2 (EZH2) was frequently observed in patients with resected small cell lung cancer (SCLC) , but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.

EZH2, a target of miR-144, serves as an oncogene in LUAD. EZH2 was upregulated in lung adenocarcinoma (LUAD) cells. Its knockdown could suppress the propagation and invasion of LUAD cells.

EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequently than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.

Ezh2 inhibition may restrict cell proliferation and promote defined adaptive responses. Targeting these responses potentially improves outcomes in Kras-driven non-small-cell lung cancers.

these results indicate that changes in EZH2 expression lead to changes in CEP55 expression in lung adenocarcinoma, and these changes are associated with its prognosis

Results found that EZH2 overexpression was significantly correlated with poor disease-free and overall survival of patients with lung adenocarcinoma. Also, EZH2 was shown to be an independent predictor of EMT marker expression, Vimentin, and vice versa.

LncRNA MSTO2P promotes proliferation and autophagy of lung cancer cells by up-regulating EZH2 expression.

The present results indicate that EZH2 regulates the immunosuppressive molecule PD-L1 expression via HIF-1alpha in non-small cell lung cancer cells.

High EZH2 expression is associated with non-small cell lung cancer.

LINC00511 promotes the progression of non-small cell lung cancer through downregulating LATS2 and KLF2 by binding to EZH2 and LSD1.

MicroRNA-130-5p promotes invasion as well as migration of lung adenocarcinoma cells by targeting the EZH2 signaling pathway.

High EZH2 expression is associated with non-small cell lung cancer.

EZH2 enhances expression of CCL5 to promote recruitment of macrophages and invasion in lung cancer.

Enhancer of zeste homolog 2 (EZH2) interacts with 3'-end of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and knockdown of MALAT1 disrupts occupancy of EZH2 on miR-22 promoter. Cooperating with EZH2, MALAT1 positively regulated snail family transcriptional repressor 1 (SNAI1) by repressing miR-22 and inhibiting E-cadherin expression, playing a vital role in epithelial to mesenchymal transition.

Exosome-transmitted lncRNA UFC1 promotes non-small-cell lung cancer progression by EZH2-mediated epigenetic silencing of PTEN expression.

MiR-92b inhibits proliferation and invasion of lung cancer by targeting EZH2.

Decreased miR-124 contributes to the epithelial-mesenchymal transition phenotype formation of lung adenocarcinoma cells via targeting enhancer of zeste homolog 2.

CAMK2A supported tumor initiating cells of lung adenocarcinoma by upregulating SOX2 through EZH2 phosphorylation.

Loss of histone lysine methyltransferase EZH2 confers resistance to tyrosine kinase inhibitors in non-small cell lung cancer.