Epigenetic reprogramming and post-transcriptional regulation during the epithelial–mesenchymal transition

2012 ◽  
Vol 28 (9) ◽  
pp. 454-463 ◽  
Author(s):  
Chung-Yin Wu ◽  
Ya-Ping Tsai ◽  
Min-Zu Wu ◽  
Shu-Chun Teng ◽  
Kou-Juey Wu
Keyword(s):  
Transcriptional Regulation ◽  
Epithelial Mesenchymal Transition ◽  
Epigenetic Reprogramming ◽  
Mesenchymal Transition ◽  
Post Transcriptional Regulation

SETD1A to induce epithelial-mesenchymal transition to promote invasion and metastasis through epigenetic reprogramming of snail in gastric cancer.

2021 ◽  
Vol 39 (3_suppl) ◽  
pp. 241-241
Author(s):  
Jugang Wu ◽  
Jiwei Yu ◽  
Yan Gu
Keyword(s):  
Gastric Cancer ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Epigenetic Modification ◽  
Epigenetic Reprogramming ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
E Cadherin

241 Background: Aberrant epigenetic modification induces oncogenes expression and promotes cancer development. The histone lysine methyltransferase SETD1A, which specifically methylates H3K4, is involved in tumor growth and metastasis, and its ectopic expression has been detected in aggressive malignancies. Our previous study had reported that SETD1A promoted gastric cancer (GC) proliferation and tumorigenesis. However, the function and molecular mechanisms of SETD1A in GC metastasis remain to be elucidated. Methods: Transwell migration and invasion assay were performed to determine GC cell migration and invasion. Lung metastasis assay was used to detect GC cell metastasis. Western Blot and Real-time qPCR were performed to measure the protein and mRNA levels, respectively. ChIP assay was performed to investigate the methylation of H3K4. The correlation between SETD1A and EMT associated key genes in GC were performed by bioinformatic analysis. Results: In this study, we found that overexpression of SETD1A promotes GC migration and invasion, whereas knockdown of SETD1A suppressed GC migration, invasion and metastasis. Furthermore, knockdown of SETD1A suppressed GC epithelial-mesenchymal transition (EMT) by increasing the expression of epithelial marker E-cadherin, and decreasing the expression of mesenchymal markers, including N-cadherin, Fibronectin and Vimentin. Mechanistically, knockdown of SETD1A reduced the EMT key transcriptional factors snail. SETD1A was recruited to the promoter of snail, where SETD1A could methylate H3K4. However, knockdown of SETD1A decreased the methylation of H3K4 on snail promoter. Rescue of snail restored SETD1A knockdown-induced GC migration and invasion inhibition. In addition, linear correlation between SETD1A and several key EMT genes, including E-cadherin, Fibronectin and snail, in GC specimens obtained from TCGA dataset. Conclusions: In summary, our data reveals that SETD1A mediated EMT process and induced metastasis through epigenetic reprogramming of snail.

scholarly journals Metformin regulates breast cancer stem cello ntogeny by transcriptional regulation of the epithelial-mesenchymal transition (EMT) status

Cell Cycle ◽  
2010 ◽  
Vol 9 (18) ◽  
pp. 3831-3838 ◽  
Author(s):  
Alejandro Vazquez-Martin ◽  
Cristina Oliveras-Ferraros ◽  
Sílvia Cufí ◽  
Sonia Del Barco ◽  
Begoña Martin-Castillo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcriptional Regulation ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals MicroRNAs regulate the epithelial–mesenchymal transition and influence breast cancer invasion and metastasis

Tumor Biology ◽  
2017 ◽  
Vol 39 (2) ◽  
pp. 101042831769168 ◽  
Author(s):  
Min Zhao ◽  
Lin Ang ◽  
Jin Huang ◽  
Jin Wang
Keyword(s):  
Breast Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Invasion ◽  
Invasion And Metastasis ◽  
Mesenchymal Phenotype ◽  
Mesenchymal Transition ◽  
Rna Molecules ◽  
Breast Cancer Invasion ◽  
Proliferation And Apoptosis ◽  
Post Transcriptional Regulation

MicroRNAs are small RNA molecules that play a major role in the post-transcriptional regulation of genes and influence the development, differentiation, proliferation, and apoptosis of cells and the development and progression of tumors. The epithelial–mesenchymal transition is a process by which epithelial cells morphologically transform into cells with a mesenchymal phenotype. The epithelial–mesenchymal transition plays a highly important role in tumor invasion and metastasis. Increasing evidence indicates that microRNAs are tightly associated with epithelial–mesenchymal transition regulation in tumor cells. In breast cancer, various microRNA molecules have been identified as epithelial–mesenchymal transition inducers or inhibitors, which, through different mechanisms and signaling pathways, participate in the regulation of breast cancer invasion and metastasis among various biological behaviors. The epithelial–mesenchymal transition–related microRNAs in breast cancer provide valuable molecules for researching cell invasion and metastasis, and they also provide candidate targets that may be significant for the targeted therapy of breast cancer.

MicroRNA-Mediated Post-Transcriptional Regulation of Epithelial to Mesenchymal Transition in Cancer

2016 ◽  
Vol 23 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Golnoush Dehbashi Behbahani ◽  
Nastaran Mohammadi Ghahhari ◽  
Mohammad Amin Javidi ◽  
Asghar Farzi Molan ◽  
Neda Feizi ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Post Transcriptional Regulation
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