Department of Radiotherapy, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China.
Biosci Rep. 2020 Oct 30;40(10). doi: 10.1042/BSR20190701.
Lung cancer (LC) is characterized by high morbidity and mortality. Numerous long noncoding RNAs (lncRNAs) have been reported to be involved in the initiation and progression of human cancers, including LC. Long intergenic non-protein coding RNA 205 (LINC00205) is identified as a novel lncRNA, which has only been unmasked to be a potential cancer promoter in hepatocellular carcinoma and pancreatic cancer. The biologic function and the molecular mechanism of LINC00205 in LC require to be investigated. In the present study, we observed the elevated expression of LINC00205 in LC tissues and cells through real-time quantitative PCR (RT-qPCR). Additionally, silencing LINC00205 inhibited LC cell growth and migration, but aggravated cell apoptosis. Moreover, we found that LINC00205 recruited FUS to maintain the mRNA stability of cold shock domain containing E1 (CSDE1) and therefore up-regulated CSDE1 expression in LC. Further, the effects of LINC00205 on LC cell proliferation, apoptosis and migration were all erased by CSDE1 overexpression. These findings demonstrated that LINC00205 facilitates malignant phenotypes in LC by recruiting FUS to stabilize CSDE1, suggesting LINC00205 as a potential target for LC therapy.
肺癌（LC）的特点是发病率和死亡率高。大量的长非编码 RNA（lncRNA）已被报道参与人类癌症的发生和发展，包括 LC。长基因间非蛋白编码 RNA 205（LINC00205）被鉴定为一种新型的 lncRNA，仅在肝癌和胰腺癌中被揭示为潜在的癌症促进因子。LINC00205 在 LC 中的生物学功能和分子机制需要进一步研究。在本研究中，我们通过实时定量 PCR（RT-qPCR）观察到 LINC00205 在 LC 组织和细胞中的表达升高。此外，沉默 LINC00205 抑制 LC 细胞的生长和迁移，但加重细胞凋亡。此外，我们发现 LINC00205 招募 FUS 来维持冷休克域包含 E1（CSDE1）的 mRNA 稳定性，从而在上调 LC 中 CSDE1 的表达。此外，CSDE1 的过表达消除了 LINC00205 对 LC 细胞增殖、凋亡和迁移的影响。这些发现表明，LINC00205 通过招募 FUS 稳定 CSDE1 促进 LC 中的恶性表型，提示 LINC00205 可能成为 LC 治疗的潜在靶点。
