CircABCB10 promotes nonsmall cell lung cancer cell proliferation and migration by regulating the miR‐1252/FOXR2 axis. Issue 3 (11th November 2018)

• Record Type: Journal Article
• Authors: Tian, Xufeng; Zhang, Lin; Jiao, Yan; Chen, Junsheng; Shan, Ying; Yang, Wenfeng
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 3(2019)
• Page Start: 3765
• Page End: 3772
• Publication Date: 2018-11-11
• Subjects: circABCB10 -- FOXR2 -- miR‐1252 -- nonsmall cell lung cancer -- proliferation and migration; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27657
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: Circular RNA (circRNA) is a key regulator in the development and progression of human cancers. Previous studies confirmed circRNA‐0008717 (circABCB10) as an oncogene in osteosarcoma, but the regulatory effect of circABCB10 in nonsmall cell lung cancer (NSCLC) is still unclear. In the current study, we examined the expression of circABCB10 in different NSCLC cell lines. Bioinformatics analysis, Cell Counting Kit‐8 assays, Transwell migration, fluorescein reporting experiments, and xenografts in mice were used to detect the effect of circABCB10 on NSCLC cell proliferation and migration in vitro and tumor growth in vivo. The results showed that the expression of circABCB10 in NSCLC cell lines was increased. Downregulation of circABCB10 suppressed NSCLC cell proliferation and migration by promoting microRNA miR‐1252 expression and suppressing Forkhead box 2 (FOXR2). Fluorescein reporting experiments confirmed that circABCB10 expression increased FOXR2 levels by sponging miR‐1252, and in vivo experiments found that knockdown of circABCB10 decreased tumor growth. These data suggested that circABCB10 acted as a tumor promoter through a novel miR‐1252/FOXR2 axis, providing potential biomarkers and therapeutic targets for the management of NSCLC. Abstract : 1. CircABCB10 acted as a tumor promoter. 2. Downregulation of circABCB10 suppressed nonsmall cell lung cancer cell proliferation and migration by promoting microRNA miR‐1252 expression and suppressing Forkhead box 2.