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DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation

Endometrial carcinoma (EC) is one of the most common gynecologic malignancy, but molecular mechanisms of the development and progression of EC remain unclear. Here we showed that the expression of DICER1 was negatively associated with the level of histone methylation, histone acetylation and PRC2 co...

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Autores principales: Li, Bilan, Lu, Wen, Qu, Junjie, Zhang, Yongli, Wan, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436244/
https://www.ncbi.nlm.nih.gov/pubmed/28529604
http://dx.doi.org/10.7150/jca.17435
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author Li, Bilan
Lu, Wen
Qu, Junjie
Zhang, Yongli
Wan, Xiaoping
author_facet Li, Bilan
Lu, Wen
Qu, Junjie
Zhang, Yongli
Wan, Xiaoping
author_sort Li, Bilan
collection PubMed
description Endometrial carcinoma (EC) is one of the most common gynecologic malignancy, but molecular mechanisms of the development and progression of EC remain unclear. Here we showed that the expression of DICER1 was negatively associated with the level of histone methylation, histone acetylation and PRC2 components SUZ12 and EZH2 in EC cells. In addition, knockdown of DICER1 significantly downregulated miR-200b and let-7i, which may then regulate their targets SUZ12 and EZH2. Furthermore, knockdown of DICER1 remarkably suppressed the expression of epithelial cell marker E-cadherin, induced the expression of mesenchymal cell marker Vimentin, and promoted the invasion of EC cells. In conclusion, our data suggest that DICER1 suppresses SUZ12 and EZH2 via affecting their upstream miRNA synthesis, and inhibits epithelial-mesenchymal transition(EMT) and invasion of EC cells via histone modification.
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spelling pubmed-54362442017-05-19 DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation Li, Bilan Lu, Wen Qu, Junjie Zhang, Yongli Wan, Xiaoping J Cancer Research Paper Endometrial carcinoma (EC) is one of the most common gynecologic malignancy, but molecular mechanisms of the development and progression of EC remain unclear. Here we showed that the expression of DICER1 was negatively associated with the level of histone methylation, histone acetylation and PRC2 components SUZ12 and EZH2 in EC cells. In addition, knockdown of DICER1 significantly downregulated miR-200b and let-7i, which may then regulate their targets SUZ12 and EZH2. Furthermore, knockdown of DICER1 remarkably suppressed the expression of epithelial cell marker E-cadherin, induced the expression of mesenchymal cell marker Vimentin, and promoted the invasion of EC cells. In conclusion, our data suggest that DICER1 suppresses SUZ12 and EZH2 via affecting their upstream miRNA synthesis, and inhibits epithelial-mesenchymal transition(EMT) and invasion of EC cells via histone modification. Ivyspring International Publisher 2017-03-12 /pmc/articles/PMC5436244/ /pubmed/28529604 http://dx.doi.org/10.7150/jca.17435 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Li, Bilan
Lu, Wen
Qu, Junjie
Zhang, Yongli
Wan, Xiaoping
DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title_full DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title_fullStr DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title_full_unstemmed DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title_short DICER1 regulates endometrial carcinoma invasion via histone acetylation and methylation
title_sort dicer1 regulates endometrial carcinoma invasion via histone acetylation and methylation
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436244/
https://www.ncbi.nlm.nih.gov/pubmed/28529604
http://dx.doi.org/10.7150/jca.17435
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