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Copyright (c) 2025 Zhi Xing, Shajidan Abudureyimu, Palida Abulaiti, Yu Wang, Hui Li, Maolin Lyu, Ying Gao
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.LncRNA MEG3 overexpression modulates proliferation without inducing apoptosis in rat cardiomyoblast h9c2 cells: a transcriptomic approach
Corresponding Author(s) : Ying Gao
Cellular and Molecular Biology,
Vol. 71 No. 9: Issue 9
Abstract
Long non-coding RNAs (lncRNAs) have been implicated in various biological processes including cell proliferation and apoptosis. However, the role of lncRNA-MEG3 in rat cardiomyoblast H9C2 cells remains unclear. In this study, H9C2 cells were genetically modified to overexpress lncRNA MEG3. The proliferation of these cells was evaluated using the Cell Counting Kit-8 (CCK-8) assay and direct imaging techniques. Apoptosis was assessed through flow cytometry, employing Annexin V and propidium iodide (PI) staining. Quantitative PCR was utilized to confirm the overexpression of lncRNA MEG3. Further, differential expression and alternative splicing analyses were conducted using comprehensive transcriptome sequencing. The overexpression of lncRNA MEG3 in H9C2 cells led to a significant reduction in cell proliferation, as evidenced by lower absorbance readings in the CCK-8 assay and reduced cell confluency in imaging analyses. However, flow cytometric analysis revealed no substantial differences in apoptosis between the lncRNA MEG3 overexpressing group and the control. Transcriptomic analyses demonstrated significant changes in gene expression and alternative splicing patterns, highlighting the intricate role of lncRNA MEG3 in cellular regulatory mechanisms. In conclusion, lncRNA MEG3 overexpression in rat cardiomyoblast H9C2 cells significantly inhibits cellular proliferation without markedly inducing apoptosis, suggesting a specific regulatory role in cellular growth processes. The transcriptomic alterations observed underscore the potential of lncRNA MEG3 as a key player in the molecular dynamics of cardiomyoblasts.
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