GliomamiR-92b-王坤课件.pptVIP

miR-92b controls glioma malignancy Dr. Kun Wang, Prof. Yirong Wang Department of neurosurgery, SRRSH Hospital Introduction- GBM One of the most common forms of neural malignancy. Median survival of 9-12 months. Poor prognosis. Mechanism? Wnt/β-catenin signaling, NLK and GBM GBM Function as oncogenes or tumor suppressor genes MicroRNA microRNA Wnt/β-catenin signaling Wnt/β-catenin signaling Nemo-like kinase miR-92b ? Objective To identify a concrete mechanism of Wnt/beta-catenin pathway regulation by microRNAs in glioma. Materials and methods Human glioblastoma cell lines: U251, U87, LN229, SNB19 and A172. Glioma samples: 9 normal brain tissues, 14 low grade gliomas (grade I and II) and 24 high grade gliomas (grade III and IV) miR-92b inhibitor: 5′-GGAGGCCGGGACGAGUGCAAUA-3′ Materials and methods qRT-PCR, Western blot analysis. MTT assay, Flowcytometry, Transwell assay, Wound healing assay and Annexin V staining. Results (qRT-PCR) Results (qRT-PCR) Results (qRT-PCR and Western Blot) Results (MTT assay) Results (Flowcytometry) Results (Wound healing assay) Results (Transwell assay) Results (Prediction) Targetscan, MiRanda Pictar Conclusion and Discussion The expression of miR-92b was elevated in both glioma samples and glioma cells. Down-regulation of miR-92b triggered growth inhibition, induced apoptosis, and suppressed invasion of glioma in vitro. NLK is potential target of miR-92b. MiR-92b inhibitor might serve as a glioma therapeutic agent To be continued…… miR-92b controls glioma malignancy through regulating Wnt/beta-catenin signaling via NLK. Experiment in vivo. Clinical significance.