Yang Longhai, Li Lili, Zhou Zizi, Liu Yi, Sun Jinyuan, Zhang Xiaoming, Pan Huiyu, Liu Song
1Department of Cardiothoracic Surgery, Shenzhen University General Hospital/Shenzhen University Clinical Medical Academy, No. 1098 Xueyuan Road, Xili University Town, Shenzhen, 518055 Guangdong China.
2Respiratory Medicine, Liaocheng People's Hospital of Shandong Province, Liaocheng, 252000 Shandong China.
Cancer Cell Int. 2020 Jan 23;20:24. doi: 10.1186/s12935-020-1099-0. eCollection 2020.
Increasing evidences have underlined the importance of long non-coding RNAs (lncRNAs) in human malignancies. LINC00958 has been found involved in some cancers. However, the underlying mechanical performance of LINC00958 in lung adenocarcinoma (LAD) has not been explored yet.
The expression of relevant mRNA and protein were measured by qRT-PCR and western blot assays. EdU, colony formation, TUNEL and transwell assays were performed to investigate the function of LINC00958 on LAD progression. Luciferase reporter, RNA pull down and RIP assays were conducted to investigate the molecular mechanism of relevant RNAs.
LINC00958 was found notably overexpressed in LAD, which was associated with the stimulation of its promoter activity induced by SP1. LINC00958 depletion dramatically inhibited LAD cell proliferation, migration and invasion capacities by acting as a miR-625-5p sponge. MiR-625-5p curbed LAD progression via targeting CPSF7 and down-regulating its expression. Mechanically, LINC00958 was identified as a competing endogenous RNA (ceRNA) and positively regulated the expression of CPSF7 via sponging miR-625-5p.
LINC00958 might drive LAD progression via mediating miR-625-5p/CPSF7 axis, indicating the potential of targeting LINC00958 for the treatment of LAD.
越来越多的证据强调了长链非编码RNA（lncRNAs）在人类恶性肿瘤中的重要性。已发现LINC00958与某些癌症有关。然而，LINC00958在肺腺癌（LAD）中的潜在作用机制尚未得到探索。
通过qRT-PCR和蛋白质免疫印迹法检测相关mRNA和蛋白质的表达。进行EdU、集落形成、TUNEL和Transwell实验以研究LINC00958对LAD进展的作用。进行荧光素酶报告基因、RNA下拉和RIP实验以研究相关RNA的分子机制。
发现LINC00958在LAD中显著过表达，这与其启动子活性受SP1诱导有关。LINC00958的缺失通过充当miR-625-5p的海绵显著抑制了LAD细胞的增殖、迁移和侵袭能力。miR-625-5p通过靶向CPSF7并下调其表达来抑制LAD进展。机制上，LINC00958被鉴定为一种竞争性内源RNA（ceRNA），并通过海绵吸附miR-625-5p正向调节CPSF7的表达。
LINC00958可能通过介导miR-625-5p/CPSF7轴推动LAD进展，这表明靶向LINC00958治疗LAD具有潜力。
