Exosomes from glioma cells induce a tumor-like phenotype in mesenchymal stem cells by activating glycolysis.

摘要: Exosomes are nanoscale membrane vesicles secreted by both normal and cancer cells, cell-derived exosomes play an important role in the cross-talk between cells other cellular components tumor microenvironment. Mesenchymal stem (MSCs) have tropism for tumors been used as tumor-tropic vectors therapy; however, safety of such therapeutic use MSCs is unknown. In this study, we investigated glioma tumor-like phenotype transformation human bone marrow mesenchymal (hBMSCs) explored underlying molecular mechanisms. The effect from U251 on growth hBMSCs was evaluated with CCK-8 assay, KI67 staining, a cell cycle distribution assessment. migration invasion were Transwell assay. A proteomics bioinformatics approach, together Western blotting reverse transcriptase-polymerase chain reaction, to investigate proteome hBMSCs. induced enhancing their proliferation, migration, altering production proteins involved regulation cycle. Moreover, promoted metastasis-related MMP-2 MMP-9, marker GFAP, CSC markers (CD133 Nestin). ten differentially expressed identified participated several biological processes exhibited various functions, mainly related inactivation glycolysis. showed that upregulated levels Glut-1, HK-2, PKM-2, leading induction glucose consumption generation lactate ATP. Treatment 2-deoxy-d-glucose significantly reversed these effects Our data demonstrate activate glycolysis hBMSCs, resulting transformation. This suggests interfering interaction microenvironment has potential approach glioma. ᅟ