Preclinical ReportsLncRNA MEG8 promotes tumor progression of non-small cell lung cancer via regulating miR-107/CDK6 axisLiu, Yinga; Li, Leib; Shang, Pengc; Song, XiangaAuthor Information aDepartment of Oncology, The Second Hospital of Shanxi Medical University bDepartment of Radiotherapy, People’s Hospital of Shanxi Province cDepartment of Orthopedics, Shanxi Dayi Hospital, Taiyuan, Shanxi, China Received 19 November 2019 Revised form accepted 10 June 2020 Correspondence to Xiang Song, Department of Oncology, the Second Hospital of Shanxi Medical University, No. 382, Wuyi Road, Xinghualing District, Taiyuan, Shanxi 030001, China, Tel: +86 13803436909; e-mail: [email protected] Anti-Cancer Drugs: November 2020 - Volume 31 - Issue 10 - p 1065-1073 doi: 10.1097/CAD.0000000000000970 Buy Metrics Abstract Mounting evidence has implicated the vital role of long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC). This study aims to investigate the mechanism of lncRNA MEG8 on NSCLC progression. The mRNA expressions of MEG8 and miR-107 were examined in tumor and adjacent normal tissues from patients with NSCLC by qRT-PCR. Lung epithelial BEAS-2B cells were transfected with MEG8 overexpression plasmid, and NSCLC A549 and H1299 cells were transfected with MEG8 or miR-107 overexpression/knockdown plasmid to detect the function of MEG8 or miR-107 on cell activity. The function of MEG8 and miR-107 on cell proliferation, cell cycle changes, invasion and migration was separately determined by Cell counting kit-8 assay and 5-ethynyl-2’-deoxyuridine staining, flow cytometry, transwell and cell scratch test. Target sites for miR-107 and MEG8, miR-107 and CDK6 were determined and verified by a dual luciferase gene reporter assay. The expression levels of the Rb/E2F3 signal pathway related proteins (p21, p27, E2F3 and Rb) were inspected by Western blot. MEG8 was strongly expressed while miR-107 was lowly expressed in tumor tissues and cells. Overexpression of MEG8 potentiated cell proliferation, migration and invasion in BEAS-2B cells. Silencing MEG8 or overexpression of miR-107 clearly hindered cell progression in A549 and H1299 cells. Mechanistically, MEG8 and CDK6 can competitively bind to miR-107 and together regulate the progression of NSCLC. Additionally, silencing MEG8 or overexpression of miR-107 can inhibit the phosphorylation levels of Rb and E2F3. Evidence in this work indicated that MEG8 regulates miR-107/CDK6 axis to promote NSCLC progression by activating the Rb/E2F3 pathway. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.