Taken together, our study clarified that the HOTAIR/miR-126/GLS pathway is involved in glioma progression and may potentially serve as a target for glioma therapy.
The miR-126 expression is abnormally low in glioma cells, and miR-126 inhibits the course of glioma through targeted regulation of PTEN/PI3K/Akt and MDM2-p53 pathways, which, therefore, can be used as a new potential biomarker for the diagnosis, treatment and prognosis of glioma.
We aimed to explore the relationship between miR-126 and glioma. miR-126 was highly expressed in low-grade clinical glioma tissue samples but lowly expressed in high-grade ones (P < .01).
In the present study, we aimed to verify the miRNA-126 down-regulation which showed in the results of glioma tissue miRNAs chip and discuss the miRNA-126 methylation in patients with glioma.
Taken together, these findings showed that miR-126 functions as a tumor suppressor in glioma cells by targeting IRS-1 expression via the PI3K/AKT signaling pathways, suggesting that miR-126 might be a novel target for therapeutic strategies in glioma.
Taken together, we concluded that miR-126 enhances the formation of glioma cancer stem cell probably via down regulation of IRS-1 in neurotrophin signaling pathway.
Many microRNAs (miRNAs) such as miR-183, miR-9, miR-137 and miR-126 expression change may be involved in the cross talk between glioma prevalence and schizophrenia.
Kirsten rat sarcoma viral oncogene (KRAS) which is involved in ERK pathway was directly targeted by miR-126 in glioma through binding to two sites in the 3' untranslated region (3'-UTR) of KRAS mRNA.