About Enhancer
| Enhancer ID: | E_01_0544 |
| Species: | human |
| Position : | chr12:2956550-2958550   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Lung adenocarcinoma (lad) |
| Pubmed ID: | 29667772 |
| Enhancer experiment: | Tissue microarray (TMA),immunohistochemical (IHC) staining, small interfering RNA(siRNA) transfection,Quantitative reverse transcription-PCR,MTT,Transwell assays,Western blot, Flow cytometric analyses,Luciferase activity assays, |
| Enhancer experiment description: | Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction. |
About Target gene
| Target gene : | -- |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction. |
About TF
| TF name : | TEAD4(EFTR-2,RTEF1,TCF13L1,TEF-3,TEF3,TEFR-1,hRTEF-1B) |
| TF experiment: | Tissue microarray (TMA),immunohistochemical (IHC) staining, small interfering RNA(siRNA) transfection,Quantitative reverse transcription-PCR,MTT,Transwell assays,Western blot, Flow cytometric analyses,Luciferase activity assays, |
| TF experiment description: | Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction. |
About Function
| Enhancer function : | Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction. |
| Enhancer function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction. |
About SNP
| SNP ID: | -- |
Upstream Pathway Annotation of TF
| GeneName | Pathway Name | Source | Gene Number |
|---|---|---|---|
| TEAD4 | PPARA activates gene expression | reactome | 113 |
| TEAD4 | YAP1- and WWTR1 (TAZ)-stimulated gene expression | reactome | 29 |
| TEAD4 | Hs_VEGFA-VEGFR2_Signaling_Pathway_WP3888_90000 | wikipathways | 153 |
Enhancer associated network
The number on yellow line represents the distance between enhancer and
target gene