Open AccessA novel antisense lncRNA NT5E promotes progression by modulating the expression of SYNCRIP and predicts a poor prognosis in pancreatic cancer
Author(s) -
Zhang Pengbo,
Cao Meng,
Zhang Yi,
Xu Lei,
Meng Fanchao,
Wu Xinquan,
Xia Tianfang,
Chen Qun,
Shi Guodong,
Wu Pengfei,
Chen Lei,
Lu Zipeng,
Yin Jie,
Cai Baobao,
Cao Shouji,
Miao Yi,
Jiang Kuirong
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15718
Subject(s) - gene knockdown , carcinogenesis , cancer research , biology , cell growth , in vivo , pancreatic cancer , cell migration , luciferase , cell culture , in vitro , epithelial–mesenchymal transition , reporter gene , cell , microbiology and biotechnology , cancer , transfection , gene expression , metastasis , gene , biochemistry , genetics
A novel antisense lncRNA NT5E was identified in a previous microarray that was clearly up‐regulated in pancreatic cancer (PC) tissues. However, its biological function remains unclear. Thus, we aimed to explore its function and clinical significance in PC. The lncNT5E expression was determined in PC specimens and cell lines. In vitro and in vivo studies detected the impact of lncNT5E depletion on PC cell proliferation, migration and invasion. Western blotting investigated the epithelial‐mesenchymal transition (EMT) markers. The interaction between lncNT5E and the promoter region of SYNCRIP was detected by dual‐luciferase reporter assay. The role of lncNT5E in modulating SYNCRIP was investigated in vitro. Our results showed that lncNT5E was significantly up‐regulated in PC tissues and cell lines and associated with poor prognosis. LncNT5E depletion inhibited PC cell proliferation, migration, invasion and EMT in vitro and caused tumorigenesis arrest in vivo. Furthermore, SYNCRIP knockdown had effects similar to those of lncNT5E depletion. A significant positive relationship was observed between lncNT5E and SYNCRIP. Moreover, the dual‐luciferase reporter assays indicated that lncNT5E depletion significantly inhibited SYNCRIP promoter activity. Importantly, the malignant phenotypes of lncNT5E depletion were rescued by overexpressing SYNCRIP. In conclusion, lncNT5E predicts poor prognosis and promotes PC progression by modulating SYNCRIP expression.