ArticleCell proliferation2020
The overexpression of long intergenic ncRNA00162 induced by RelA/p65 promotes growth of pancreatic ductal adenocarcinoma.
Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- A novel long non-coding RNA, PICSAR, promotes thyroid cancer progression through the hsa-miR-320A/hsa-miR-485/RAPGEFL1 axis.Medical oncology (Northwood, London, England) · 2025Article
- LINC00162 regulates cell proliferation and apoptosis by sponging PAQR4-targeting miR-485-5p.Journal of cellular physiology · 2022Article
- Emerging Roles of Long Non-Coding RNAs in Ankylosing Spondylitis.Frontiers in immunology · 2022Review
- Duhuo Jisheng Decoction inhibits the activity of osteoclasts in osteonecrosis of the femoral head via regulation of the RELA/AKT1 axis.American journal of translational research · 2022Article
- RELA-induced MiR-21 Exerts Oncogenic Effects on PDAC via Targeting of ARHGAP24.Journal of Cancer · 2022Article
- The overexpression of long intergenic ncRNA00162 induced by RelA/p65 promotes growth of pancreatic ductal adenocarcinoma.Cell proliferation · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesRecent 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
methodsIn 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.
resultsThese 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.
conclusionsIn sum, our results provide first evidence for the role of LINC00162 in promoting PDAC progression and the potential underlying mechanism of LINC00162 overexpression.
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