We concluded MiR-34a-5p suppressed tumorigenesis and progression of glioma and potentiated TMZ-induced cytotoxicity for glioma cells by targeting HMGA2, deepening our understanding on molecular basis of HMGA2 in glioma.
Reverse transcription‑quantitative polymerase chain reaction was used to analyze the expression of MMP‑9 and microRNA‑34a (miR‑34a) in the plasma of patients with glioma and healthy volunteers.
In conclusion, the results demonstrated a novel role for miR‑34a, inducing glioma cell senescence, whereas miR‑34a modulation of SIRT1, inducing DNA damage, is crucial for miRNA replacement therapy in glioma treatment.
QRT-PCR and western blot were used to measure the relative expression levels of circNFIX, miR-34a-5p and <i>NOTCH</i> and identify their correlation in glioma.
Long non-coding RNA antisense non-coding RNA in the INK4 locus (ANRIL) variants are associated with glioma and miR-34a is markedly downregulated in U251 glioma cells.
In addition, miR-34a overexpression significantly down-regulates the expression and distribution of tight junction-related proteins in glioma endothelial cells (GECs), paralleled by protein kinase Cε (PKCε) reduction.
The insensitivity of glioma to standard therapies combined with the hypothesis that glioma stem cells (GSCs) are responsible for this chemorefractory nature suggests that investigations exploring the function and mechanism of miR-34a in GSCs would be of value.