Department of Respiratory Medicine, Jining First People's Hospital, Jining, 272000, Shandong, China.
Department of Respiratory Medicine, Jining First People's Hospital, Jining, 272000, Shandong, China.
Biochem Biophys Res Commun. 2019 Jun 25;514(2):443-449. doi: 10.1016/j.bbrc.2019.04.132. Epub 2019 May 1.
The non-small cell lung cancer (NSCLC) denotes a malignant type of cancers. Long non-coding RNAs (lncRNAs) can actively participate in cancer development. However, the exact role of lncRNAs in NSCLC remains largely elusive. In current work, we report a novel intergenic lncRNA LINC01288 involved in NSCLC. We found that LINC01288 is frequently upregulated in NSCLC samples and cell lines. LINC01288 significantly promotes viability, migration, xenograft tumor growth and metastasis in vitro and in vivo. LINC01288 physically interacts with the IL-6 mRNA and increase the stability of IL-6 transcripts. Subsequently, the autocrine induction of IL-6 and enhanced STAT3 activation may facilitate NSCLC progression. Collectively, our data have demonstrated that LINC01288 serves as a crucial mediator of IL-6/STAT3 pathway and created novel interplay between lncRNAs and tumor development.
非小细胞肺癌（NSCLC）是一种恶性癌症。长链非编码 RNA（lncRNA）可以积极参与癌症的发展。然而，lncRNA 在 NSCLC 中的确切作用在很大程度上仍不清楚。在当前的工作中，我们报告了一种新型的参与 NSCLC 的基因间 lncRNA LINC01288。我们发现 LINC01288 在 NSCLC 样本和细胞系中经常上调。LINC01288 显著促进 NSCLC 的体外和体内的活力、迁移、异种移植肿瘤生长和转移。LINC01288 与 IL-6 mRNA 物理相互作用，并增加 IL-6 转录本的稳定性。随后，IL-6 的自分泌诱导和增强的 STAT3 激活可能促进 NSCLC 的进展。总之，我们的数据表明 LINC01288 作为 IL-6/STAT3 通路的关键介质，并在 lncRNA 和肿瘤发展之间创造了新的相互作用。
