[No authors listed]
MicroRNAâ432 (miRâ432) has been studied in multiple tumors, but the expression status, biological functions and the mechanism of action of miRâ432 in glioblastoma multiforme (GBM) are yet to be elucidated. In the present study, miRâ432 expression in GBM was determined and its clinical significance was evaluated among patients with GBM. The effects on the malignancy of GBM in vitro and in vivo were examined in detail and the interactions between miRâ432 and insulinâlike growth factor 1 receptor (IGFâ1R) mRNA were then explored. miRâ432 expression in GBM tissue samples and cell lines was measured by reverse transcriptionâquantitative (RTâq)PCR. GBM cell proliferation, apoptosis, migration and invasion in vitro and tumor growth in vivo were evaluated by a Cell Counting Kitâ8 assay, flowâcytometric analysis, Transwell migration and invasion assays, and a tumor xenograft experiment, respectively. Bioinformatic analysis followed by a luciferase reporter assay, RTâqPCR and western blotting was applied to demonstrate that IGFâ1R is a direct target gene of miRâ432 in GBM cells. It was found that miRâ432 is downregulated in GBM tumors and cell lines. miRâ432 under expression obviously correlated with the Karnofsky Performance Status score and shorter overall survival among patients with GBM. Exogenous miRâ432 expression significantly reduced proliferation and induced apoptosis of GBM cells. In addition, miRâ432 overexpression impaired the migratory and invasive abilities of GBM cells in vitro and decreased their tumor growth in vivo. Furthermore, IGFâ1R was validated as a direct target gene of miRâ432 in GBM cells. IGFâ1R knockdown imitated the tumorâsuppressive actions of miRâ432 overexpression in GBM cells. Rescue experiments proved IGFâ1R downregulation to be essential for the effects of miRâ432 on GBM cells. The results of the present study revealed a tumorâsuppressive role of the miRâ432âIGFâ1R axis in GBM cells and this axis may have implications for GBM therapy.
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