Artikel
Influence of miRNA-219 on HMGA2 Gene expression and survival in human glioblastoma cells
Die Wirkung der miRNA-219 auf die Expression von HMGA2 und das Überleben von Glioblastomzellen
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Veröffentlicht: | 25. Mai 2022 |
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Gliederung
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Objective: High-mobility group AT-hook protein 2 (HMGA2) is a transcription factor that leads to tumor progression and cell proliferation in several types of cancer. We could recently show, that HMGA2 is overexpressed in human glioblastoma (GBM) and a higher HMGA2-expression is associated with worse prognosis. The miRNA-219 targets HMGA2 and downregulates its expression, leading to tumor suppression and growth inhibition in various cancer cells. This study aims to investigate the influence of miRNA-219 on HMGA2-expression and cell survival in human glioblastoma cells.
Methods: G28 and A172 cells were cultured and transfected with the mirVana™ hsa-miR-219a-5p micro-RNA-Inhibitor or a miR-219a-5p mimic (both Life Technologies, Thermo Fisher [HG1]). After 48 hours RNA was isolated and expression of HMGA2 and miR-219 was examined by quantitative real-time-PCR and cell survival was investigated by CellTiter-Glo 2.0 ATP-Assay (Promega) and FACS analysis.
Results: In both GBM-cell lines miR-219 expression was downregulated after transfection with the miR-219a-5p micro-RNA-Inhibitor and upregulated after transfection with the miRNA-219 mimic. In G28 HMGA2-expression was increased after transfection with the miRNA-219 inhibitor, while the mimic did not show an influence on HMGA2-gene-expression. In A172 cells HMGA2-expression could be downregulated with the miRNA-219 mimic, but no influence of the miRNA-219 inhibitor could be observed. There was no difference in cell survival in G28 cells. A172 cells that were transfected with the miRNA-219 mimic showed increased survival compared to A172 cells treated with the miRNA-219 inhibitor.
Conclusion: In both investigated cell lines miRNA-219 transfection led to a change of HMGA2-gene-expression. Cell survival, however, could not be impaired by HMGA2 downregulation. These results suggest that there is an influence of miRNA-219 on HMGA2-expression in human GBM cells. Contrary to our assumption HMGA2 downregulation did not decrease cell survival. This implies that HMGA2 mediated tumor progression might happen via different mechanisms of action.