Department of Oncology, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12741-12747. doi: 10.26355/eurrev_202012_24173.
This study aims to explore the cancer-associated functions of microRNA-587 (miR-587) in the development of non-small-cell lung carcinoma (NSCLC) and the molecular mechanism.
Relative expression levels of miR-587 and CYLD in NSCLC samples were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Proliferative and migratory abilities in A549 and H1299 cells with overexpressed miR-587 were examined by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. The regulatory interaction between miR-587 and CYLD was determined by Dual-Luciferase reporter assay and Pearson correlation test. At last, the co-regulation of miR-587 and CYLD on NSCLC cell functions was assessed by rescue experiments.
MiR-587 was upregulated in NSCLC samples and closely linked to tumor staging, whereas CYLD was downregulated and negatively correlated to that of miR-587. Survival analysis suggested that miR-587 was an unfavorable factor to the prognosis of NSCLC. Overexpression of miR-587 stimulated proliferative and migratory abilities in A549 and H1299 cells. CYLD was the downstream gene binding miR-587. Overexpression of CYLD could partially abolish the regulatory effects of overexpressed miR-587 on promoting proliferative and migratory abilities in NSCLC cells.
MiR-587 stimulates proliferative and migratory abilities in NSCLC by downregulating CYLD, thus aggravating the progression of NSCLC.
本研究旨在探讨 microRNA-587（miR-587）在非小细胞肺癌（NSCLC）发生发展中的癌相关功能及其分子机制。
采用实时定量聚合酶链反应（qRT-PCR）检测 NSCLC 样本中 miR-587 和 CYLD 的相对表达水平。通过细胞计数试剂盒（CCK-8）和 Transwell 检测过表达 miR-587 的 A549 和 H1299 细胞的增殖和迁移能力。通过双荧光素酶报告基因检测和 Pearson 相关检验确定 miR-587 和 CYLD 之间的调控相互作用。最后，通过 rescue 实验评估 miR-587 和 CYLD 对 NSCLC 细胞功能的共同调控作用。
miR-587 在 NSCLC 样本中上调，与肿瘤分期密切相关，而 CYLD 下调，与 miR-587 呈负相关。生存分析表明 miR-587 是 NSCLC 预后的不利因素。过表达 miR-587 可刺激 A549 和 H1299 细胞的增殖和迁移能力。CYLD 是 miR-587 的下游靶基因。过表达 CYLD 可部分消除过表达 miR-587 对促进 NSCLC 细胞增殖和迁移能力的调节作用。
miR-587 通过下调 CYLD 刺激 NSCLC 的增殖和迁移能力，从而加重 NSCLC 的进展。
