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Copyright (c) 2022 Ming Zhu, Mengwei Tian, Fazhen Xu, Yuting Huang, Jiantian Yang
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.Long non-coding RNA XIST negatively regulates thoracic aortic aneurysm cell proliferation by targeting the miR-193a-5p/KLF7 axis
Corresponding Author(s) : Ming Zhu
Cellular and Molecular Biology,
Vol. 68 No. 7: Issue 7
Abstract
Non-coding RNAs (ncRNAs) are important molecular modulators in diverse pathological processes, influencing the occurrence and progression of carcinomas. Thoracic aortic aneurysm (TAA) is an infrequent disease among aneurysmal diseases and accounts for nearly 3% of diagnosed aneurysms. The functional roles of long ncRNA (lncRNA) XIST and miR-193a-5p and the associated molecular mechanisms are yet to be investigated. In the current study, we discovered that miR-193a-5p was expressed at low levels in the blood of TAA patients. Further, loss-of-function and gain-of-function assays disclosed that miR-195-3p impacted the proliferation ability of TAA cells. XIST was found to be the most overexpressed lncRNA among predicted lncRNAs binding to miR-193a-5p. The promotive function of XIST in TAA was also explored. Subsequently, KLF7 was proved to be the downstream factor of the XIST/miR-193a-5p axis. Rescue assays testified the whole regulation mechanism of the XIST/miR-193a-5p/KLF7 axis in TAA. MiR-193a-5p was absorbed by XIST for the improvement of KLF7 in TAA. These results concluded that XIST might be engaged in TAA pathogenesis via regulation of the miR-193a-5p/KLF7 axis, supplementing more therapeutic options for TAA treatment.
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