Meng Fanmei, Zhou Yijing, Dong Baohua, Dong Aiqin, Zhang Jingtao
Outpatient Department, Dongying District People's Hospital, 333 Jinan Road, Dongying, 257085, Shandong, China.
Department of Respiratory Medicine, Dongying District People's Hospital, 333 Jinan Road, Dongying, Shandong, China.
Cancer Cell Int. 2020 Dec 7;20(1):588. doi: 10.1186/s12935-020-01680-3.
It is increasingly evidenced that long non-coding RNAs (lncRNAs) play an important role in various diseases. LncRNA LINC01194 acts as an oncogene in several cancer types. Nevertheless, the role of LINC01194 in lung adenocarcinoma (LUAD) has not yet been revealed.
qRT-PCR was used to detect the expression of LINC01194, miR-641 and SETD7 mRNA, while western blot was exploited to examine SETD7 protein level. Cell proliferation was detected by colony formation and EdU assays. Transwell assays detected cell migration and invasion. TUNEL assay and flow cytometry analysis were used to detect cell apoptosis. RIP, RNA pull down and luciferase reporter assays detected the binding among LINC01194, miR-641 and SETD7.
LINC01194 was significantly upregulated in LUAD tissues and cell lines. Knockdown of LINC01194 resulted in decreased cell proliferation, migration and invasion, and increased apoptosis. Mechanistic experiments unveiled that LINC01194 augmented SETD7 expression in LUAD cells by competitively interacting with miR-641. Rescue experiments showed that miR-641 inhibition and SETD7 overexpression rescued the repressing impacts on LUAD cell proliferation, migration and invasion caused by LINC01194 knockdown.
LINC01194 promotes the progression of LUAD by enhancing miR-641-targeted SETD7. The LINC01194/miR-641/SETD7 axis might provide new molecular targets for treating LUAD.
越来越多的证据表明，长链非编码RNA（lncRNA）在各种疾病中发挥着重要作用。lncRNA LINC01194在几种癌症类型中充当癌基因。然而，LINC01194在肺腺癌（LUAD）中的作用尚未明确。
采用qRT-PCR检测LINC01194、miR-641和SETD7 mRNA的表达，同时利用蛋白质免疫印迹法检测SETD7蛋白水平。通过集落形成实验和EdU实验检测细胞增殖。Transwell实验检测细胞迁移和侵袭。TUNEL实验和流式细胞术分析用于检测细胞凋亡。RIP、RNA下拉实验和荧光素酶报告基因实验检测LINC01194、miR-641和SETD7之间的相互作用。
LINC01194在LUAD组织和细胞系中显著上调。敲低LINC01194导致细胞增殖、迁移和侵袭能力下降，凋亡增加。机制实验表明，LINC01194通过与miR-641竞争性相互作用增强LUAD细胞中SETD7的表达。挽救实验表明，抑制miR-641和过表达SETD7可挽救因敲低LINC01194对LUAD细胞增殖、迁移和侵袭的抑制作用。
LINC01194通过增强miR-641靶向的SETD7促进LUAD进展。LINC01194/miR-641/SETD7轴可能为治疗LUAD提供新的分子靶点。
