Function And Mechanism Of MicroRNA-23a In Glioma Cells

MicroRNAs (miRNAs) is an endogenous noncoding RNA which is about22nucleotides in length. It could regulate the expression of mRNA through degradingthe target mRNA or inhibiting the translation of the target mRNA. Abnormalexpression of miRNAs is closely related with human tumors. Recently, manystudies reported that miRNAs could regulate cell proliferation, apoptosis andvariation during cell development.Glioma is the most common malignant tumor, which mechanism is complicated.In the past30years, the diagnosis and treatment of glioma has made great progress.For example, molecular biology and genetics study have identified that the natureand the biological behavior of some glioma were benign, such as cilia astrocytomawhich prognosis is good; some biological sensitive markers of malignant glioma tochemotherapy and radiotherapy had been found, such as promoter methylation ofMGMT gene, heterozygosity loss of chromosome1p and chromosome19q; morethan47gene had mutated in glioblastoma multiforme (GBM) which had benddetected by The Cancer Genome Atlas (TCGA).The miRNA which is a non-coding RNA gene is always expression out of thecontrol in glioma. The high-throughput chip techonology and Northern blot wereused to analyze the many potential cancer miRNAs (onco-miRNAs) expression inglioma tissues and glioma cell lines. The results showed that the expression ofmiR-23a in glioma tissues and cell lines was significantly upregulation. The results of QRT-PCR showed that the expression of miR-23a in100glioma tissues wasupregulation compared with the matched normal tissue. It indicated that miR-23amay play an important role in the tumorigenesis of gliomas as onco-miRNA.To investigate the function of miR-23a, we used the anti-miR-23a in glioma cellsto inhibit its expression, and then the phenotype of glioma cell lines U87wasanalyzed. The results showed that glioma cell proliferation had decreased after theuse of anti-miR-23a. We used the bioinformatics and molecular biology toinvestigate the expression of its target genes. The results showed that APAF1is animportant target gene for regulation. Overexpression of APAF1could inhibit cellproliferation and promote cell apoptosis in U87. We think that miR-23a couldinhibit the expression of APAF1and play the function of oncogenes, whichdecrease apoptosis of glioma cells and promote the proliferation and cell cycle.In summary, miR-23a and its target genes constitute a complicated regulationnetwork, which plays an important role in the oncogenes of gliomas. Theexpression inhibition of miR-23a may provide a new effective strategy for gliomatreatment.