MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1

MiR-200a has been reported to be able to suppress the epithelial-mesenchymal transition process in pancreatic cancer stem cells, suggesting that miR-200a could suppress the metastasis of pancreatic ductal adenocarcinoma (PDAC). However, its role in proliferation and metastasis of PDAC and the underl...

Full description

Bibliographic Details
Main Authors: Wu, Xiaoyu, Wu, Guannan, Wu, Zhenfeng, Yao, Xuequan, Li, Gang
Format: Online
Language:English
Published: Neoplasia Press 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800058/
id pubmed-4800058
recordtype oai_dc
spelling pubmed-48000582016-04-05 MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1 Wu, Xiaoyu Wu, Guannan Wu, Zhenfeng Yao, Xuequan Li, Gang Original article MiR-200a has been reported to be able to suppress the epithelial-mesenchymal transition process in pancreatic cancer stem cells, suggesting that miR-200a could suppress the metastasis of pancreatic ductal adenocarcinoma (PDAC). However, its role in proliferation and metastasis of PDAC and the underlying mechanism by which miR-200a works in PDAC have not been elucidated. In our study, we for the first time identified that DEK gene is a direct downstream target of miR-200a. It was found that overexpression of miR-200a decreased DEK expression, suppressing the proliferation, migration, and invasion of PDAC cells. Meanwhile, knockdown of miR-200a can increase DEK level, promoting the proliferation, migration, and invasion of PDAC cells. Our study demonstrated that miR-200a suppresses the metastasis in pancreatic PDAC through downregulation of DEK, suggesting that miR-200a may be used as a novel potential marker in prediction of metastasis of PDAC. Neoplasia Press 2016-03-03 /pmc/articles/PMC4800058/ /pubmed/26947878 http://dx.doi.org/10.1016/j.tranon.2015.11.005 Text en © 2016 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Wu, Xiaoyu
Wu, Guannan
Wu, Zhenfeng
Yao, Xuequan
Li, Gang
spellingShingle Wu, Xiaoyu
Wu, Guannan
Wu, Zhenfeng
Yao, Xuequan
Li, Gang
MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
author_facet Wu, Xiaoyu
Wu, Guannan
Wu, Zhenfeng
Yao, Xuequan
Li, Gang
author_sort Wu, Xiaoyu
title MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
title_short MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
title_full MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
title_fullStr MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
title_full_unstemmed MiR-200a Suppresses the Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma through Downregulation of DEK Gene1
title_sort mir-200a suppresses the proliferation and metastasis in pancreatic ductal adenocarcinoma through downregulation of dek gene1
description MiR-200a has been reported to be able to suppress the epithelial-mesenchymal transition process in pancreatic cancer stem cells, suggesting that miR-200a could suppress the metastasis of pancreatic ductal adenocarcinoma (PDAC). However, its role in proliferation and metastasis of PDAC and the underlying mechanism by which miR-200a works in PDAC have not been elucidated. In our study, we for the first time identified that DEK gene is a direct downstream target of miR-200a. It was found that overexpression of miR-200a decreased DEK expression, suppressing the proliferation, migration, and invasion of PDAC cells. Meanwhile, knockdown of miR-200a can increase DEK level, promoting the proliferation, migration, and invasion of PDAC cells. Our study demonstrated that miR-200a suppresses the metastasis in pancreatic PDAC through downregulation of DEK, suggesting that miR-200a may be used as a novel potential marker in prediction of metastasis of PDAC.
publisher Neoplasia Press
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800058/
_version_ 1613555139561390080