The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.
1/5 보강
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).
APA
Karimian F, Loghmani Z, et al. (2025). The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.. Medical oncology (Northwood, London, England), 42(12), 544. https://doi.org/10.1007/s12032-025-03103-7
MLA
Karimian F, et al.. "The potential role of BM-MSC-derived exosomes in TUG1 modulation: antileukemic effects on THP-1 cells.." Medical oncology (Northwood, London, England), vol. 42, no. 12, 2025, pp. 544.
PMID
41212348 ↗
Abstract 한글 요약
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.
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