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Copyright © 2022 Yan Liang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0/

Abstract

Background. The purpose of this study was to explore the functions of FOXD2-AS1 and miR-31 in retinoblastoma. Material and Methods. An RT-qPCR assay was applied to calculate the mRNA levels of FOXD2-AS1, miR-31, and PAX9. A dual-luciferase reporter gene assay was employed to verify the connection between FOXD2-AS1, miR-31, and PAX9 expression. Results. FOXD2-AS1 was upregulated, and miR-31 was lowly expressed in retinoblastoma. Low expression of FOXD2-AS1 promoted cell proliferation and migration, and upregulation of FOXD2-AS1 inhibited proliferative and migratory abilities. lncRNA FOXD2-AS1 directly bound to miR-31 and regulated miR-31 expression in SO-RB50 cells. Cell proliferation and migration were inhibited by the miR-31 mimic. miR-31 mediated PAX9 expression via directly binding to PAX9 mRNA. A miR-31 inhibitor partially reversed the effect of FOXD2-AS1 knockdown on the proliferation and migration in SO-RB50 cells. FOXD2-AS1 knockdown reduced PAX9 expression in SO-RB50 cells. PAX9 had negative connection with miR-31, and it had positive relationship with FOXD2-AS1. Conclusion. lncRNA FOXD2-AS1 inhibited cell proliferation and migration via the miRNA-31/PAX9 axis in retinoblastoma.

Details

Title
lncRNA FOXD2-AS1 Promotes the Retinoblastoma Cell Viability and Migration by Sponging miR-31
Author
Liang, Yan 1 ; Wang, Hong 1 ; Song, Ruiying 1 ; Yin, Xiuyan 1   VIAFID ORCID Logo 

 Department of Ophthalmology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000 Shandong Province, China 
Editor
Yue Gu
Publication year
2022
Publication date
2022
Publisher
John Wiley & Sons, Inc.
ISSN
23146133
e-ISSN
23146141
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2683808422
Copyright
Copyright © 2022 Yan Liang et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0/