Open AccessThe overexpression of long intergenic ncRNA00162 induced by RelA/p65 promotes growth of pancreatic ductal adenocarcinoma
Author(s) -
Lu Yu,
Wu Min,
Fu Jie,
Sun Yichen,
Furukawa Kenei,
Ling Jianhua,
Qin Xue,
Chiao Paul J.
Publication year - 2020
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12805
Subject(s) - cancer research , downregulation and upregulation , chromatin immunoprecipitation , biology , cell growth , pancreatic cancer , long non coding rna , in vivo , cell culture , pancreatic ductal adenocarcinoma , cancer , gene , gene expression , genetics , promoter
Objectives Recent observations have emphasized the role of long non‐coding RNA (lncRNA) in cancer progression; however, a genetic profile of lncRNAs in pancreatic ductal adenocarcinoma (PDAC) remains an ongoing study. Materials and Methods In this research, RNA sequencing showed that LINC00162 is dramatically increased in patient‐derived tumour cell lines (PATC) compared with the human pancreatic nestin‐positive epithelial (HPNE) cells. Results These data were validated in several PDAC cell lines, and significant upregulation of LINC00162 was found in all of them. Knock‐down of LINC00162 significantly inhibited the proliferation, colony formation and migration of PATC cells in vitro and suppressed the growth of PATC xenografts in vivo. Overexpression of LINC00162 in PDAC cell lines (AsPc‐1) showed consistent results, with significantly increased proliferation, colony formation and migration of AsPc‐1 cells, as well as enhanced tumour growth of the AsPc‐1 xenografts in vivo. Furthermore, the result of Chromatin immunoprecipitation assay revealed that RelA/p65 directly bound to LINC00162, and the expression of LINC00162 in PDAC decreased after RelA/p65 knock‐down, the proliferation ability of AsPc‐1 also significantly inhibited after knocking down LINC00162 and RelA/p65 simultaneously, indicating that RelA/p65 directly involve in the transcriptional regulation of LINC00162. Conclusions In sum, our results provide first evidence for the role of LINC00162 in promoting PDAC progression and the potential underlying mechanism of LINC00162 overexpression.