LncRNA FEZF1-AS1 Sponges miR-34a to Upregulate Notch-1 in Glioblastoma
Authors Luo L, Zhang Y, He H, Chen C, Zhang B, Cai M
Received 29 November 2019
Accepted for publication 16 February 2020
Published 11 March 2020 Volume 2020:12 Pages 1827—1833
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Chien-Feng Li
Lun Luo,1 Yuan Zhang,2 Haiyong He,1 Chuan Chen,1 Baoyu Zhang,1 Meiqin Cai1
1Department of Neurosurgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province 510630, People’s Republic of China; 2Department of Obstetrics, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province 510630, People’s Republic of China
Correspondence: Lun Luo; Meiqin Cai
Department of Neurosurgery, The Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Tianhe District, Guangzhou, Guangdong Province 510630, People’s Republic of China
Email firstname.lastname@example.org; email@example.com
Introduction: LncRNA FEZF1-AS1 has been reported to be an oncogene in many types of cancer, while its role in glioblastoma (GBM) is unknown. This study aimed to investigate the potential involvement of FEZF1-AS1 in GBM.
Methods: FEZF1-AS1 expression in paired GBM and non-tumor tissues from GBM patients was determined by RT-qPCR. A 2-year follow-up was performed to analyze the prognostic value of FEZF1-AS1 for GBM. Cell transfections were performed to analyze the interactions between FEZF1-AS1, miR-34a and Notch-1. Transwell assay was performed to analyze the role of FEZF1-AS1, miR-34a and Notch-1 in regulating GBM cell invasion and migration.
Results: In this study, analysis of TCGA dataset revealed the upregulation of FEZF1-AS1 in GBM, and the overexpression of FEZF1-AS1 in GBM was further confirmed using GBM tissues from GBM patients included in this study. High levels of FEZF1-AS1 were correlated with poor survival. FEZF1-AS1 was predicted to form base pairing with miR-34a. However, overexpression of FEZF1-AS1 and miR-34a failed to affect the expression of each other. However, upregulation of Notch-1, a target of miR-34a, was observed after FEZF1-AS1 in GBM cells. Moreover, increased invasion and migration rates of GBM cells were observed after FEZF1-AS1 and Notch-1 overexpression. MiR-34a played an opposite role and reduced the effects of FEZF1-AS1 and Notch-1 overexpression.
Conclusion: FEZF1-AS1 may sponge miR-34a to upregulate Notch-1 in GBM, thereby promoting cancer cell invasion and migration.
Keywords: glioblastoma, FEZF1-AS1, miR-34a, Notch-1
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