Huang Xiuming, Huang Mingfang, Chen Minbiao, Chen Xianshan
Department of Thoracic Surgery, Hainan General Hospital, Haikou, Hainan, 570311, People's Republic of China.
Cancer Manag Res. 2022 Mar 9;14:1087-1098. doi: 10.2147/CMAR.S352308. eCollection 2022.
Non-small cell lung cancer (NSCLC) is a prevalent type of lung cancer worldwide. Long noncoding RNA (lncRNA) SLC9A3-AS1 is reported to play a carcinogenic role in nasopharyngeal carcinoma, but its full-scale role in NSCLC remains elusive.
SLC9A3-AS1 expression was detected in serum and tissue of NSLCC patients and NSCLC cell lines. The effects of SLC9A3-AS1 on NSCLC proliferation, migration and invasion were evaluated using CCK-8 and transwell assays. In addition, the potential downstream molecules of SLC9A3-AS1 were searched and explored by bioinformatics analysis, RT-qPCR, dual-luciferase reporter, and rescue experiments.
SLC9A3-AS1 was upregulated in NSCLC tissues and cell lines. SLC9A3-AS1 possessed a favorable ability in diagnosing NSCLC. A high level of SLC9A3-AS1 was associated with poor prognosis in NSCLC patients. Functionally, SLC9A3-AS1 knockdown inhibited cell proliferation, migration, and invasion of NSCLC cells. Mechanistically, SLC9A3-AS1 acted as competing endogenous RNA for miR-760 to regulate NSCLC progression. In addition, rescue assay showed that downregulation of miR-760 could reverse the modulatory activity of SLC9A3-AS1 knockdown on NSCLC cells.
SLC9A3-AS1 was upregulated in NSCLC, and SLC9A3-AS1 knockdown hindered NSCLC progression through targeting miR-760, suggesting that it may prove to be a novel biomarker and therapeutic target for NSCLC.
非小细胞肺癌(NSCLC)是全球范围内一种常见的肺癌类型。据报道,长链非编码RNA(lncRNA)SLC9A3-AS1在鼻咽癌中发挥致癌作用,但其在NSCLC中的全面作用仍不清楚。
检测NSLCC患者血清和组织以及NSCLC细胞系中SLC9A3-AS1的表达。使用CCK-8和transwell实验评估SLC9A3-AS1对NSCLC增殖、迁移和侵袭的影响。此外,通过生物信息学分析、RT-qPCR、双荧光素酶报告基因和拯救实验搜索并探索SLC9A3-AS1潜在的下游分子。
SLC9A3-AS1在NSCLC组织和细胞系中上调。SLC9A3-AS1具有良好的NSCLC诊断能力。高水平的SLC9A3-AS1与NSCLC患者的不良预后相关。在功能上,SLC9A3-AS1敲低抑制了NSCLC细胞的增殖、迁移和侵袭。机制上,SLC9A3-AS1作为miR-760的竞争性内源RNA来调节NSCLC进展。此外,拯救实验表明miR-760的下调可逆转SLC9A3-AS1敲低对NSCLC细胞的调节活性。
SLC9A3-AS1在NSCLC中上调,SLC9A3-AS1敲低通过靶向miR-760阻碍NSCLC进展,表明它可能是NSCLC的一种新型生物标志物和治疗靶点。