Department of Pulmonary and Critical Care Medicine, Qingdao Municipal Hospital, Qingdao, Shandong, China.
Health Office, Qingdao Municipal Hospital, Qingdao, Shandong, China.
Aging (Albany NY). 2020 Nov 5;12(22):22582-22598. doi: 10.18632/aging.103833.
Increasing evidence confirms that long noncoding RNAs (lncRNAs) exert vital functions in multiple biological process among malignant cancers. In the current study, we uncovered that linc00968 was downregulated in lung adenocarcinoma (LUAD). Furthermore, the low level of linc00968 was correlated with worse prognosis in patients with LUAD. Upregulation of linc00968 restrained the growth and metastatic phenotypes of LUAD cell and . Using bioinformation methods and luciferase reporter assay, we identified that linc00968 acted as a competing endogenous RNA (ceRNA) via sponging miR-9-5p to modulate the level of Cytoplasmic Polyadenylation Element Binding Protein 3 (CPEB3) in LUAD. In addition, LUAD cell migration, colony formation and epithelial-mesenchymal transition (EMT) process were suppressed by linc00968 while these aggressive traits were reversed by miR-142-5p or CPEB3 silencing. Altogether, our work disclosed that linc00968 played a critical role in LUAD and linc00968/miR-9-5p/CPEB3 regulatory axis might be a potential treatment target in LUAD.
越来越多的证据证实,长非编码 RNA(lncRNA)在多种恶性肿瘤的生物学过程中发挥着重要作用。在本研究中,我们发现 linc00968 在肺腺癌(LUAD)中表达下调。此外,linc00968 的低水平与 LUAD 患者的预后较差相关。上调 linc00968 抑制了 LUAD 细胞的生长和转移表型。利用生物信息学方法和荧光素酶报告基因实验,我们发现 linc00968 通过海绵吸附 miR-9-5p 作为竞争性内源 RNA(ceRNA)来调节 LUAD 中细胞质多聚腺苷酸化元件结合蛋白 3(CPEB3)的水平。此外,linc00968 抑制 LUAD 细胞迁移、集落形成和上皮-间充质转化(EMT)过程,而 miR-142-5p 或 CPEB3 沉默则逆转了这些侵袭性特征。总之,我们的工作揭示了 linc00968 在 LUAD 中的关键作用,linc00968/miR-9-5p/CPEB3 调控轴可能是 LUAD 的潜在治疗靶点。