1. Down-regulation of miR-106b suppresses the growth of human glioma cells.
- Author
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Zhang A, Hao J, Wang K, Huang Q, Yu K, Kang C, Wang G, Jia Z, Han L, and Pu P
- Subjects
- Animals, Apoptosis, Blotting, Western, Brain Neoplasms genetics, Brain Neoplasms pathology, Female, Flow Cytometry, Glioma genetics, Glioma pathology, Humans, In Situ Hybridization, Mice, Mice, Inbred BALB C, Mice, Nude, Neoplasm Grading, Oligonucleotides, Antisense pharmacology, Prognosis, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Retinoblastoma Protein genetics, Retinoblastoma Protein metabolism, Retinoblastoma-Like Protein p107 genetics, Retinoblastoma-Like Protein p107 metabolism, Retinoblastoma-Like Protein p130 genetics, Retinoblastoma-Like Protein p130 metabolism, Reverse Transcriptase Polymerase Chain Reaction, Tissue Array Analysis, Xenograft Model Antitumor Assays, Brain Neoplasms prevention & control, Cell Proliferation, Gene Expression Regulation, Neoplastic, Glioma prevention & control, MicroRNAs genetics
- Abstract
Recently, many studies have found that the miR-106b ~25 cluster plays an oncogenic role in tumor progression. However, the precise role of each microRNAs (miRNAs) in the cluster is not yet clear. In the present study, we examined the expression of miR-106b in glioma samples and a tissue microarray by real-time PCR and in situ hybridization (ISH), respectively, finding that miR-106b is overexpressed in the majority of gliomas. Meanwhile, the expression of miR-106b was positively correlated with tumor grade (p < 0.05). The transfection of a miR-106b anti-sense oligonucleotide (ASON) into three human glioma cell lines (U251, LN229 and TJ905) suppressed the proliferation of these cells. Moreover, the growth of xenograft tumors in nude mice treated with miR-106b ASON was significantly impaired. A bioinformatics analysis predicted that RBL2 may be the target of miR-106b, and dual-luciferase reporter assays identified RBL2, but not RB1 or RBL1, as a target of miR-106b. These results suggest that miR-106b facilitates glioma cell growth by promoting cell cycle progression through the negative regulation of RBL2.
- Published
- 2013
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