LncRNA MEG3 overexpression modulates proliferation without inducing apoptosis in rat cardiomyoblast h9c2 cells: a transcriptomic approach.

Zhi Xing, Shajidan Abudureyimu, Palida Abulaiti, Yu Wang, Hui Li, Maolin Lyu, Ying Gao
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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.

LncRNA MEG3过表达调节大鼠成心肌细胞h9c2细胞增殖而不诱导凋亡:转录组学方法
长链非编码rna (lncRNAs)参与多种生物过程,包括细胞增殖和凋亡。然而,lncRNA-MEG3在大鼠成心肌细胞H9C2中的作用尚不清楚。本研究对H9C2细胞进行基因修饰,使其过表达lncRNA MEG3。使用细胞计数试剂盒-8 (CCK-8)测定和直接成像技术评估这些细胞的增殖。采用膜联蛋白V和碘化丙啶(PI)染色,流式细胞术检测细胞凋亡。利用定量PCR证实lncRNA MEG3过表达。此外,利用综合转录组测序进行了差异表达和选择性剪接分析。lncRNA MEG3在H9C2细胞中的过表达导致细胞增殖显著减少,CCK-8检测中吸光度读数降低,成像分析中细胞融合度降低。然而,流式细胞术分析显示lncRNA MEG3过表达组与对照组之间的细胞凋亡无显著差异。转录组学分析显示了基因表达和剪接模式的显著变化,突出了lncRNA MEG3在细胞调节机制中的复杂作用。综上所述,lncRNA MEG3在大鼠成心肌细胞H9C2中过表达可显著抑制细胞增殖,但不显著诱导细胞凋亡,提示其在细胞生长过程中具有特异性调控作用。观察到的转录组学改变强调了lncRNA MEG3在心肌细胞分子动力学中的关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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