LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma
Objective: To investigate the underlying mechanism of lncRNA TUG1 in pancreatic ductal adenocarcinoma (PDAC). Methods: The expression of TUG1 was defined by qRT-PCR. The apoptotic cells were detected by flow cytometry assay. The cell migration and invasion were measured by scratch assay and Transwel...
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doaj-eeed0722de8f479a95167f63c7ae9ec22020-11-24T21:38:03ZengElsevierJournal of Pharmacological Sciences1347-86132018-06-011372116121LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinomaFan Yang0Xiaofang Li1Lingjuan Zhang2Lina Cheng3Xiuling Li4Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, ChinaDepartment of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, ChinaDepartment of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, ChinaDepartment of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, ChinaCorresponding author. Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, No.7 Weiwu Road, Zhengzhou, 450003, Henan, People's Republic of China.; Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, ChinaObjective: To investigate the underlying mechanism of lncRNA TUG1 in pancreatic ductal adenocarcinoma (PDAC). Methods: The expression of TUG1 was defined by qRT-PCR. The apoptotic cells were detected by flow cytometry assay. The cell migration and invasion were measured by scratch assay and Transwell assay. The level of ERK pathway was detected using Western blot. Results: Compared with normal tissues and cells, the expression of TUG1 was up-regulated in pancreatic cancer tissue and cells. Meanwhile, knockdown of TUG1 could promote PDAC cells apoptosis and inhibit PDAC cells viability, migration and invasion. In addition, overexpression of TUG1 enhanced the gemcitabine chemoresistance of PDAC cells. Surprisingly, gemcitabine combined with SCH772984 (a suppressor of ERK pathway) could reverse the drug resistance resulted from overexpression of TUG1. Conclusion: TUG1 promoted the viability of PDAC cells and enhanced its resistance of gemcitabine. Keywords: LncRNA TUG1, PDAC, Oncogenic, Gemcitabine resistancehttp://www.sciencedirect.com/science/article/pii/S1347861318301026 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Fan Yang Xiaofang Li Lingjuan Zhang Lina Cheng Xiuling Li |
spellingShingle |
Fan Yang Xiaofang Li Lingjuan Zhang Lina Cheng Xiuling Li LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma Journal of Pharmacological Sciences |
author_facet |
Fan Yang Xiaofang Li Lingjuan Zhang Lina Cheng Xiuling Li |
author_sort |
Fan Yang |
title |
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
title_short |
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
title_full |
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
title_fullStr |
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
title_full_unstemmed |
LncRNA TUG1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
title_sort |
lncrna tug1 promoted viability and associated with gemcitabine resistant in pancreatic ductal adenocarcinoma |
publisher |
Elsevier |
series |
Journal of Pharmacological Sciences |
issn |
1347-8613 |
publishDate |
2018-06-01 |
description |
Objective: To investigate the underlying mechanism of lncRNA TUG1 in pancreatic ductal adenocarcinoma (PDAC). Methods: The expression of TUG1 was defined by qRT-PCR. The apoptotic cells were detected by flow cytometry assay. The cell migration and invasion were measured by scratch assay and Transwell assay. The level of ERK pathway was detected using Western blot. Results: Compared with normal tissues and cells, the expression of TUG1 was up-regulated in pancreatic cancer tissue and cells. Meanwhile, knockdown of TUG1 could promote PDAC cells apoptosis and inhibit PDAC cells viability, migration and invasion. In addition, overexpression of TUG1 enhanced the gemcitabine chemoresistance of PDAC cells. Surprisingly, gemcitabine combined with SCH772984 (a suppressor of ERK pathway) could reverse the drug resistance resulted from overexpression of TUG1. Conclusion: TUG1 promoted the viability of PDAC cells and enhanced its resistance of gemcitabine. Keywords: LncRNA TUG1, PDAC, Oncogenic, Gemcitabine resistance |
url |
http://www.sciencedirect.com/science/article/pii/S1347861318301026 |
work_keys_str_mv |
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