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Extracellular vesicles derived from hypoxic glioma stem-like cells confer temozolomide resistance on glioblastoma by delivering miR-30b-3p
Vesicles from low-oxygen brain tumor stem cells may cause drug resistance by delivering miR-30b-3p in glioblastoma
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Abstract
Hypoxic glioma stem-like cell-derived extracellular vesicles significantly enhance temozolomide resistance in glioblastoma cells.
- Extracellular vesicles from hypoxic glioma stem-like cells were more effective in promoting temozolomide resistance compared to those from normoxic cells.
- miR-30b-3p was found to be significantly upregulated in extracellular vesicles from hypoxic glioma stem-like cells.
- HIF1α and STAT3 were identified as transcriptional regulators of miR-30b-3p expression.
- The binding of miR-30b-3p to hnRNPA2B1 facilitated its packaging into extracellular vesicles.
- EV-packaged miR-30b-3p targeted RHOB, leading to decreased apoptosis and increased proliferation in glioblastoma cells.
- miR-30b-3p in cerebrospinal fluid may serve as a potential biomarker for predicting resistance to temozolomide.
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