Dai Jixin, Wang Bing, Zhao Yueming, Zuo Xuerong, Cui Hongxia, Chen Xi, Liu Xianhong
Department of Oncology, Jilin Cancer Hospital, Changchun, Jilin 130000, People's Republic of China.
Department of Radiotherapy, Jilin Cancer Hospital, Changchun, Jilin 130000, People's Republic of China.
Cancer Manag Res. 2020 Dec 10;12:12697-12708. doi: 10.2147/CMAR.S277113. eCollection 2020.
Recent studies have identified important roles for () in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of in NSCLC and the molecular mechanisms involved were extensively studied.
The abundance of in NSCLC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. The cell counting kit-8 assay, flow cytometry, transwell experiments for migration and invasion, and xenograft tumor model were used to assess the function of in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation.
Significant upregulation was observed in NSCLC tissues and cell lines. Silencing inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of restricted tumor growth of NSCLC cells in vivo. In addition, showed the ability to directly bind to microRNA-519d-5p (miR-519d-5p) and act as a molecular sponge for miR-519d-5p in NSCLC cells. Furthermore, the () was identified as a direct target of miR-519d-5p and could indirectly upregulate expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition.
increases expression by sequestering miR-519d-5p, thereby aggravating the malignant progression of NSCLC. The LINC01426/miR-519d-5p/ETS1 competing endogenous RNA pathway may provide a target for designing therapeutic agents for NSCLC treatment.
最近的研究已经确定了（）在胶质瘤和透明细胞肾细胞癌中的重要作用。本研究评估了（）在非小细胞肺癌（NSCLC）组织和细胞系中的表达谱。此外，还广泛研究了（）在NSCLC中的功能及其涉及的分子机制。
使用定量逆转录-聚合酶链反应测定NSCLC组织和细胞系中（）的丰度。采用细胞计数试剂盒-8检测、流式细胞术、迁移和侵袭的Transwell实验以及异种移植肿瘤模型来评估（）在NSCLC细胞中的功能。使用荧光素酶报告基因检测和RNA免疫沉淀进行机制研究。
在NSCLC组织和细胞系中观察到（）显著上调。沉默（）可抑制NSCLC细胞的增殖、迁移和侵袭，并在体外促进细胞凋亡。此外，干扰（）可在体内限制NSCLC细胞的肿瘤生长。此外，（）显示出直接结合微小RNA-519d-5p（miR-519d-5p）并在NSCLC细胞中充当miR-519d-5p分子海绵的能力。此外，（）被确定为miR-519d-5p的直接靶标，（）可通过海绵化miR-519d-5p间接上调（）表达。此外，NSCLC细胞中（）敲低的抑癌活性部分被miR-519d-5p抑制所抵消。
（）通过隔离miR-519d-5p增加（）表达，从而加重NSCLC的恶性进展。LINC01426/miR-519d-5p/ETS1竞争性内源性RNA途径可能为设计NSCLC治疗药物提供靶点。
