Copyright (c) 2023 Pan Jiang, Huabing Xia
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Circular RNA EFR3A promotes nasopharyngeal carcinoma progression through modulating the miR-654-3p/EFR3A axis
Corresponding Author(s) : Binghua Xia
Cellular and Molecular Biology,
Vol. 69 No. 12: New discoveries in gene expression and mutation
Abstract
Nasopharyngeal carcinoma (NPC) originates from the nasopharyngeal epithelium. hsa_circ_0135761 (circEFR3A), a newly identified circRNA, presented elevation in NPC via high-throughput sequencing. This study aimed to clarify the molecular mechanism of circEFR3A in the carcinogenesis of NPC. Based on RT-qPCR, subcellular fractionation, RNase R digestion and actinomycin D assays, we evaluated circEFR3A expression characteristics in NPC cells. We found that the circEFR3A was located in the cytoplasm of NPC cells, presented upregulation and stably expressed in NPC cells. Loss-of-function assays clarified the effects of circEFR3A on NPC cell malignant behaviors. The results demonstrated that circEFR3A knockdown facilitated NPC cell apoptosis but repressed NPC cell proliferation and migration. Furthermore, the regulatory mechanism of circEFR3A in NPC was explored. Bioinformatics and mechanism experiments revealed that cicrEFR3A positively modulated EFR3A by competitively binding with miR-654-3p in NPC cells. Additionally, rescue assays showed that the suppressive effects of cicrEFR3A knockdown on NPC cell proliferation, migration and apoptosis were countervailed by EFR3A upregulation. Xenograft tumor-bearing mouse models were established to investigate the role of cicrEFR3A in NPC tumorigenesis in vivo, and the results indicated that circEFR3A silencing suppressed tumor growth in mice. In conclusion, circEFR3A is highly expressed and functions as an oncogene in NPC progression. circEFR3A facilitates NPC cell proliferation and migration by binding to miR-654-3p to upregulate EFR3A, providing a potential new direction for seeking therapeutic plans for NPC.
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