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BM-MSC 来源外泌体在 TUG1 调控中的潜在作用:对 THP-1 细胞的抗白血病效应

英文原题:The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.

PubMed 2025/11/10(内容时间) Med Oncol Q2 · IF 4.7(JCR 2025)

研究概要

这些结果可能有助于阐明BM-MSC-Exos在调节白血病细胞凋亡、细胞周期进程和TUG1表达中的可能作用。

中文摘要

间充质干细胞来源外泌体(BM-MSC-Exos)因其在急性髓系白血病(AML)中调节白血病细胞行为的潜力而受到越来越多的关注。本研究评估了BM-MSC-Exos对AML细胞系THP-1的影响。MTT实验显示,处理24 h后细胞活力呈剂量依赖性降低。流式细胞术分析显示,暴露于BM-MSC-Exos后凋亡活性显著增加。细胞周期分析表明细胞在G0/G1期积累,与生长停滞一致。实时PCR基因表达谱分析显示,促凋亡基因(Caspase3、Caspase9、BID和BAX)上调,抗凋亡基因BCL2下调。同样,细胞周期调节因子如Cyclin D1和CDK6的表达也降低。重要的是,TUG1——一种与白血病发生相关的致癌长链非编码RNA——在外泌体处理的细胞中也显著下调。综上所述,这些结果可能有助于阐明BM-MSC-Exos在调节白血病细胞凋亡、细胞周期进程和TUG1表达中的可能作用。需要进一步研究以阐明这些效应背后的分子机制,并确定BM-MSC-Exos介导的TUG1调节如何参与白血病细胞调控。

展开英文摘要原文

Mesenchymal stem cell-derived exosomes (BM-MSC-Exos) have attracted increasing interest for their potential to modulate leukemic cell behavior in acute myeloid leukemia (AML). In this study, the effects of BM-MSC-Exos on the AML cell line THP-1 were evaluated. A dose-dependent reduction in cell viability was observed after 24 h of treatment, as determined by MTT assay. Flow-cytometric analysis revealed a significant increase in apoptotic activity following exposure to BM-MSC-Exos. Cell cycle analysis demonstrated an accumulation of cells in the G0/G1 phase, consistent with growth arrest. Gene-expression profiling by real-time PCR showed upregulation of pro-apoptotic genes (Caspase3, Caspase9, BID, and BAX) and downregulation of the anti-apoptotic gene BCL2. Likewise, expression of cell cycle regulators such as Cyclin D1 and CDK6 was reduced. Importantly, TUG1, an oncogenic long non-coding RNA implicated in leukemogenesis, was also significantly downregulated in exosome-treated cells. Taken together, these results may shed light on the possible role of BM-MSC-Exos in regulating apoptosis, cell-cycle progression, and TUG1 expression in leukemic cells. Further studies are warranted to elucidate the molecular mechanisms underlying these effects and to determine how BM-MSC-Exos-mediated modulation of TUG1 might contribute to leukemic cell regulation.

论文信息

作者
Karimian F、Loghmani Z、Vazifeh Shiran N、Mikanik F、Khademi M、Ahmadi A、Jalilivand S、Gharehbaghian A
第一作者单位
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Iran
通讯作者单位
Department of Laboratory Hematology and Blood Bank, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. gharehbaghian@hotmail.com.Iran
期刊
Medical oncology (Northwood, London, England)2025 Nov 10
原文标识
PubMed 41212348 · DOI 10.1007/s12032-025-03103-7