IncRNA Linc00511 Upregulation Elevates TGFBR1 and Participates in the Postoperative Distant Recurrence of Non-Small-Cell Lung Cancer by Targeting miR-98-5p.

Abstract

Long non-coding RNA (lncRNA) Linc00511 has been demonstrated as an oncogenic lncRNA in some types of cancer, such as bladder cancer and breast cancer. However, whether Linc00551 plays critical roles in non-small-cell lung cancer (NSCLC) is still unknown. To examine the role of Linc00511 in the pathogenesis of NSCLC, 62 stage I NSCLC patients and the age- and gender-matched healthy controls were enrolled in this investigation. Patients were followed up for three years. Linc00511, microRNA-98-5p (miR-98-5p) and transforming growth factor beta receptor 1 (TGFBR1) mRNA levels were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). TGFBR1 protein level was determined by Western blot. The putative interaction between Linc00511 and miR-98-5p was predicted by bioinformatics and confirmed by dual luciferase activity and RNA pull-down. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were measured by Transwell assay. Serum Linc00511 level at admission was higher in patients than in healthy controls and decreased on the day of discharge than before surgical resection. During the 3-years of follow-up, plasma Linc00511 level was upregulated only in patients with distant recurrence. Linc00511 was predicted to interact with miR-98-5p, and Linc00511 overexpression inhibited miR-98-5p expression but upregulated TGFBR1, a downstream target for miR-98-5p. Moreover, the elevation of Linc00511 and TGFBR1 both promoted NSCLC cell proliferation, invasion, and migration. However, miR-98-5p overexpression had opposite effects, reversing the effects of TGFBR1. In conclusion, Linc00511 was elevated in NSCLC, which might participate NSCLC postoperative distant recurrence and promoted NSCLC cell proliferation, migration and invasion via targeting and regulating miR-98-5p/TGFBR1 axis.