Department of Clinical Laboratory, The Sixth People's Hospital of Nantong, Yonghe road No.500, 226011, Nantong, Jiangsu, China.
Department of General Surgery, The Sixth People's Hospital of Nantong, 226011, Nantong, Jiangsu, China.
Diagn Pathol. 2021 May 22;16(1):46. doi: 10.1186/s13000-021-01108-0.
Long non-coding RNA growth arrest specific 5 (GAS5) is a regulator in non-small cell lung cancer (NSCLC) progression. Nonetheless, the mechanism by which GAS5 exerts its biological function in NSCLC cells remains unclear.
GAS5, miR-221-3p relative expression levels in NSCLC tissues and cells were examined by qPCR. After gain-of-function and loss-of-function models were established, the viability of H1299 and A549 cells were examined by CCK-8 and EdU assays. Cell migration and invasion were examined by the Transwell experiment. The binding sequence of GAS5 for miR-221-3p was confirmed by the dual-luciferase reporter gene experiment. The regulatory function of GAS5 and miR-221-3p on IRF2 was investigated by Western blot.
GAS5 expression was down-modulated in NSCLC tissues and cell lines. GAS5 overexpression restrained the proliferation, migration and invasion of NSCLC cells, while miR-221-3p, which was targeted and negatively modulated by GAS5, worked oppositely. Restoration of miR-221-3p markedly reversed the effects of GAS5 on NSCLC cells. Additionally, GAS5 increased IRF2 expression in NSCLC cells by repressing miR-221-3p.
GAS5 blocks the progression of NSCLC partly via increasing IRF2 expression level via repressing miR-221-3p.
长非编码 RNA 生长停滞特异性基因 5（GAS5）是在非小细胞肺癌（NSCLC）进展中的一种调控因子。然而，GAS5 在 NSCLC 细胞中发挥其生物学功能的机制仍不清楚。
通过 qPCR 检测 NSCLC 组织和细胞中 GAS5、miR-221-3p 的相对表达水平。建立 GAS5 过表达和敲低模型后，通过 CCK-8 和 EdU 检测 H1299 和 A549 细胞的活力。通过 Transwell 实验检测细胞迁移和侵袭。通过双荧光素酶报告基因实验验证 GAS5 与 miR-221-3p 的结合序列。通过 Western blot 研究 GAS5 和 miR-221-3p 对 IRF2 的调控作用。
GAS5 在 NSCLC 组织和细胞系中表达下调。GAS5 过表达抑制 NSCLC 细胞的增殖、迁移和侵袭，而 miR-221-3p 是 GAS5 的靶基因，受 GAS5 负调控，作用相反。miR-221-3p 的恢复显著逆转了 GAS5 对 NSCLC 细胞的影响。此外，GAS5 通过抑制 miR-221-3p 增加 NSCLC 细胞中 IRF2 的表达。
GAS5 通过抑制 miR-221-3p 增加 NSCLC 细胞中 IRF2 的表达，部分阻断 NSCLC 的进展。
