Issue
Copyright (c) 2023 Fangzhou He, Tingting Ren, Xiaodong Tang
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.METTL3-modified lncRNA-MALAT1 regulates the molecular axis of miR-124-3p/CDK4 involved in Ewing's sarcoma
Corresponding Author(s) : Xiaodong Tang
Cellular and Molecular Biology,
Vol. 69 No. 6: Issue 6
Abstract
N6-methyladenosine (m6A) modifications are considered key mechanisms in cancer. As an m6A-modified lncRNA, MALAT1 is associated with tumor progression. In this study, the MALAT1/miR-124-3p/CDK4 axis was studied to discover METTL3’s effects on Ewing's sarcoma (ES). For this purpose, clinical ES samples were collected and ES cells were cultured to detect gene expression. Then, the interlink between METTL3, MALAT1, miR-124-3p, and CDK4 was studied and confirmed, and m6A modification of MALAT1 was determined. Finally, the Transwell method was used to test migration and invasion. Results showed that ES samples expressed low miR-124-3p and high METTL3, MALAT1 and CDK4. METTL3 elevated MALAT1 expression by m6A modification. MALAT1 enhanced CDK4 expression by competing with miR-124-3p. In ES cells, METTL3 silencing repressed cell migration and invasion by inhibiting MALAT1. In conclusion, METTL3 promotes tumorigenesis of ES through the MALAT1/miR-124-3p/CDK4 axis.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX
