LncRNA LINC00520 Aggravates Cell Proliferation and Migration in Lung Adenocarcinoma via a Positive Feedback Loop

Abstract

Background: Lung adenocarcinoma (LUAD) is the most common histological subtype of primary lung cancer. Thus, to figure out the biomarker of diagnosis for LUAD is of great significance. Long non-coding RNAs (lncRNAs) are previously revealed to exert vital effects in numerous cancers. LncRNA long intergenic non-protein coding RNA 520 (LINC00520) served as an oncogene in certain cancers. Therefore, our report was specially designed to probe role of LINC00520 in LUAD. Results: LINC00520 expression was detected by RT-qPCR. Next, function of LINC00520 in LUAD was verified by in vitro loss-of-function experiments. As for LINC00520 regulatory mechanism in LUAD, we conducted pull down, ChIP, RIP, and luciferase reporter assays. We found that LINC00520 was upregulated in LUAD. Additionally, LINC00520 upregulation suggested the poorer prognosis for patients with LUAD. Furthermore, LINC00520 downregulation suppressed LUAD cell proliferation and migration and induced cell apoptosis. Simultaneously, forkhead box P3 (FOXP3) is identified as the transcription factor (TF) to transcriptionally activate LINC00520. Moreover, LINC00520 positively upregulated FOXP3 via sponging miR-3611 in LUAD. Subsequently, rescue experiments delineated that miR-3611 downregulation or FOXP3 overexpression could reverse the effect of silenced LINC00520 on proliferative and migratory capabilities in LUAD. Conclusion: This study first put forward and proved that lncRNA LINC00520 facilitated cell proliferative and migratory abilities in LUAD through interacting with miR-3611 and targeting FOXP3, which may provide a potential novel insight for treatment of LUAD.