CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
我们的工作确立了CD81作为连接放射抵抗与免疫逃逸的关键桥梁,其通过维持GBM中CD274的丰度发挥作用,并突显CD81作为优化放射免疫治疗的有前景的治疗靶点。
英文原题:The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.
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。
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。
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.
MEMBER ACCOUNT
登录成功会直接打开下一页。