CircRIP2 promotes NSCLC progression by sponging for miR-671-5p to regulate FOXM1 expression
Yizhi Liu1*, Xing Feng2*, Shuhong Kang3*, Feng Lv3*, Yunfeng Ni3 and Hua Wu4
1Department of Medical Oncology, Shaanxi Provincial Cancer Hospital, 2Nursing Department, Shaanxi Provincial Cancer Hospital, 3Department of Thoracic Surgery, Tangdu Hospital, Air Force Medical University and 4Department of Respiratory Medicine, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China
Corresponding Author: Yunfeng Ni, Department of Thoracic Surgery, Tangdu Hospital, Air Force Medical University, Xi'an 710038, PR China. e-mail: firstname.lastname@example.org or Hua Wu, Department of Respiratory Medicine, Shaanxi Provincial People's Hospital, Xi'an, 710068, Shaanxi, China. e-mail: email@example.com
Summary. Lot of attention had been paid to the role of circular RNAs (circRNAs) in carcinogenesis recently. However, knowledge about circRNAs in NSCLC development is far from satisfactory. In this study, we aimed to provide a novel insight into the circRIP2 in NSCLC development. We used NSCLC tissues, as well as cell lines to elucidate the expression and location of circRIP2 in NSCLC. We also established the circRIP2 overexpression cells A549-circRIP2 and repression cells HCC827-shcircRIP2 for further functional and mechanism studies. The pro-tumorigenic role of circRIP2 was tested by using CCK-8, BrdU and transwell assays. The interaction between circRIP2 and miR-671-5p were validated by luciferase reporter assay, RIP assay, as well as RNA pull down assay. We showed circRIP2 is differentially expressed NSCLC, and acted as a predictor for overall survival (OS) and disease-free survival (DFS). CircRIP2 promoted NSCLC progression by acting as a miRNA sponge for miR-671-5p, thus facilitating its target gene FOXM1 expression. Targeting circRIP2 could be potentially beneficial for NSCLC patients in the future. Histol Histopathol
Key words: NSCLC, circRIP2, miR-671-5p, FOXM1
©The Author(s) 2021. Open Access. This article is licensed under a Creative Commons CC-BY International License.