| Objective: Glioma is the most common primary brain tumors,which of the incidence rate is(5-8) / 1 million. Its 5-year mortality is ranked third in systemic cancer,second only to lung cancer and pancreatic cancer. It is considered that glioma is one of the major diseases of serious harm to human health. Currently, the treatment of gliomas is mainly with surgical treatment, because of the invasive growth of tumor with no obvious boundary between the brain tissues, however, all of tumor tissues cannot be removed and patients usually are with neurological deficits after surgery. In most recent 30 years,the development of clinical outcomes is limited and the survival is no significant improvement. Underlying mechanisms of glioma progression are still not fully clarified. Therefore, it is necessary that the mechanism of glioma is more further studied to discover more effective therapeutic target and treatment regimen. Circular RNAs, serve as a novel noncoding RNA, may play a critical role in biological behavior. Recently, circular RNAs are abundant in tumor cells. However, whether their expression abnormalities associate with tumor development is need to further studied. This study aims for elucidating the mechanism of effect of circular RNA CDR1 as on malignant glioma growth and providing a novel hint or strategy for the effective treatment of glioma.Methods: 1.Designed specific primer of CDR1 as based on circbase database and used RT-q PCR to detect the difference expression level of CDR1 as in glioma samples and cell line. 2. Established the CDR1 as lentivirus knockdown vector. 3. The effect of CDR1 as on proliferation was evaluated by MTT. 4. The effect of CDR1 as on cell apoptosis and cell cycle was detected by Flow-cytometric analysis. 5. p53 expression were determined by RT-q PCR and western blot after generation of stable knockdown CDR1 as.Results: 1.The lower expression of CDR1 as in glioma tissue and cell lines was detected by RT-PCR detection.2.The stable CDR1 as knockdown cell pools in U87 MGMGMG cells was successful established. 3. After transfection 48 h, MTT assay revealed that cell growth was significantly decreased in U87 MG transfected with knockdown vector of CDR1as(FG12-CDR1as) compared with controls. 4. After FG12-CDR1 as transfection 48 h, using flow cytometer to detect U87 MG apoptosis and cycle, found that compared with the control group, treatment group increased cell apoptosis, stagnation of cells in G0 / G1 phase, and the S phase decreased obviously.5. The results of RT-q PCR showed that the expression of CDR1 as was significantly decreased after transfecting FG12-CDR1 as and Western blot analysis showed that the expression of p53 was significantly decreased in U87 MG cells transfected with FG12-CDR1 as compared with control.Conclusions: Our findings suggest that CDR1 as is significantly down-regulated in glioma cell lines and tumor samples. Its inactivation may result in the promoting of cell proliferation, inhibiting apoptosis and regulating the function of the cell cycle, partially via the decreased expression of p53. |
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