Department of Clinical Laboratory, Liuzhou People's Hospital, Liuzhou, China.
Department of Molecular & Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Cell Prolif. 2020 May;53(5):e12805. doi: 10.1111/cpr.12805. Epub 2020 May 4.
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.
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.
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.
In sum, our results provide first evidence for the role of LINC00162 in promoting PDAC progression and the potential underlying mechanism of LINC00162 overexpression.
最近的观察强调了长非编码 RNA（lncRNA）在癌症进展中的作用；然而，胰腺导管腺癌（PDAC）中 lncRNA 的遗传特征仍是一个正在进行的研究。
在这项研究中，RNA 测序显示，与人胰腺巢蛋白阳性上皮（HPNE）细胞相比，LINC00162 在患者来源的肿瘤细胞系（PATC）中显著增加。
这些数据在几个 PDAC 细胞系中得到了验证，并且在所有细胞系中都发现 LINC00162 的显著上调。LINC00162 的敲低显著抑制了 PATC 细胞在体外的增殖、集落形成和迁移，并抑制了 PATC 异种移植瘤在体内的生长。LINC00162 在 PDAC 细胞系（AsPc-1）中的过表达也显示出一致的结果，AsPc-1 细胞的增殖、集落形成和迁移明显增加，AsPc-1 异种移植瘤的肿瘤生长也增强。此外，染色质免疫沉淀分析的结果表明，RelA/p65 直接与 LINC00162 结合，PDAC 中 LINC00162 的表达在 RelA/p65 敲低后降低，AsPc-1 的增殖能力在同时敲低 LINC00162 和 RelA/p65 后也显著抑制，表明 RelA/p65 直接参与 LINC00162 的转录调控。
总之，我们的结果首次提供了 LINC00162 促进 PDAC 进展的作用以及 LINC00162 过表达的潜在潜在机制的证据。
