Fan Yang1, Xiaofang Li1, Lingjuan Zhang1, Lina Cheng1, Xiuling Li2. 1. Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China. 2. Department of Gastroenterology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, 450003, China. Electronic address: xiuling_li123@sina.com.
Abstract
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.
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.
Authors: Stella Baliou; Anthony M Kyriakopoulos; Demetrios A Spandidos; Vassilios Zoumpourlis Journal: Int J Oncol Date: 2020-07-14 Impact factor: 5.650