Globally, lung cancer is known as a major cause of cancer-associated death and non-small-cell lung cancer (NSCLC) accounts for majority of all cases. Growing evidence has emerged that long non-coding RNAs (lncRNAs) act as vital regulatory molecules in various malignancies. Nevertheless, the function of SLCO4A1 antisense RNA 1(SLCO4A1-AS1) in NSCLC is vague. This study intended to investigate the biological role and probable regulatory mechanism of SLCO4A1-AS1 in NSCLC. qRT-PCR revealed that SLCO4A1-AS1 level was upregulated in NSCLC. Function assays manifested that silence of SLCO4A1-AS1 attenuated NSCLC cell proliferation, migration and invasion but promoted NSCLC cell apoptosis. Furthermore, we disclosed that SLCO4A1-AS1 activated NF-κB pathway in NSCLC, and that IKKα, an NF-κB pathway-related gene, possessed an enhanced level in NSCLC tissues and cells. Importantly, miR-223-3p bound with SLCO4A1-AS1 and IKKα. Further, SLCO4A1-AS1 competitively bound with miR-223-3p to increase IKKα expression, thereby activating NF-κB signaling pathway. In conclusion, SLCO4A1-AS1 drove NSCLC progression by activating NF-κB signaling pathway via sponging miR-223-3p to enhance IKKα expression. Thus, SLCO4A1-AS1 might be a promising biomarker for NSCLC treatment.

在全球范围内，肺癌被认为是癌症相关死亡的主要原因，非小细胞肺癌 (NSCLC) 占所有病例的大部分。越来越多的证据表明，长链非编码 RNA (lncRNA) 在各种恶性肿瘤中充当重要的调节分子。然而，SLCO4A1反义RNA 1（SLCO4A1-AS1）在NSCLC中的功能尚不清楚。本研究旨在探讨 SLCO4A1-AS1 在 NSCLC 中的生物学作用和可能的调控机制。qRT-PCR 显示 SLCO4A1-AS1 水平在 NSCLC 中上调。功能测定表明SLCO4A1-AS1的沉默减弱了NSCLC细胞的增殖、迁移和侵袭，但促进了NSCLC细胞凋亡。此外，我们公开了 SLCO4A1-AS1 激活 NSCLC 中的 NF-κB 通路，以及 IKKα，一种 NF-κB 通路相关基因，在非小细胞肺癌组织和细胞中具有增强的水平。重要的是，miR-223-3p 与 SLCO4A1-AS1 和 IKKα 结合。此外，SLCO4A1-AS1 与 miR-223-3p 竞争性结合以增加 IKKα 表达，从而激活 NF-κB 信号通路。总之，SLCO4A1-AS1 通过激活 NF-κB 信号通路通过海绵 miR-223-3p 增强 IKKα 表达来驱动 NSCLC 进展。因此，SLCO4A1-AS1 可能是 NSCLC 治疗的有希望的生物标志物。