Down-regulation of miR-106b suppresses the growth of human glioma cells

被引:30
作者
Zhang, Anling [1 ]
Hao, Jianwei [1 ]
Wang, Kun [1 ]
Huang, Qiang [1 ]
Yu, Kai [1 ]
Kang, Chunsheng [1 ]
Wang, Guangxiu [1 ]
Jia, Zhifan [1 ]
Han, Lei [1 ]
Pu, Peiyu [1 ]
机构
[1] Tianjin Med Univ Gen Hosp, Key Lab Posttrauma Neurorepair & Regenerat Cent N, Tianjin Key Lab Injuries Variat & Regenerat Nervo, Dept Neurosurg,Minist Educ,Tianjin Neurol Inst, Tianjin 300052, Peoples R China
关键词
Glioma; miR-106b Expression; miR-106b ASON; RBL2; TUMOR-SUPPRESSOR; BRAIN-TUMORS; MICRORNAS; GLIOBLASTOMA; EXPRESSION; FAMILY; CANCER; GENE; SITES; E2F1;
D O I
10.1007/s11060-013-1061-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:179 / 189
页数:11
相关论文
共 31 条
[1]  
[Anonymous], IARC CANCERBASE
[2]   Distinct recruitment of E2F family members to specific E2F-binding sites mediates activation and repression of the E2F1 promoter [J].
Araki, K ;
Nakajima, Y ;
Eto, K ;
Ikeda, MA .
ONCOGENE, 2003, 22 (48) :7632-7641
[3]   Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers [J].
Calin, GA ;
Sevignani, C ;
Dan Dumitru, C ;
Hyslop, T ;
Noch, E ;
Yendamuri, S ;
Shimizu, M ;
Rattan, S ;
Bullrich, F ;
Negrini, M ;
Croce, CM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (09) :2999-3004
[4]   MicroRNA-21 down-regulates the expression of tumor suppressor PDCD4 in human glioblastoma cell T98G [J].
Chen, Yang ;
Liu, Wei ;
Chao, Tengfei ;
Zhang, Yu ;
Yan, Xingqi ;
Gong, Yanhua ;
Qiang, Boqin ;
Yuan, Jiangang ;
Sun, Maosheng ;
Peng, Xiaozhong .
CANCER LETTERS, 2008, 272 (02) :197-205
[5]   Extensive modulation of a set of microRNAs in primary glioblastoma [J].
Ciafrè, SA ;
Galardi, S ;
Mangiola, A ;
Ferracin, M ;
Liu, CG ;
Sabatino, G ;
Negrini, M ;
Maira, G ;
Croce, CM ;
Farace, MG .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2005, 334 (04) :1351-1358
[6]   Pocket proteins and cell cycle control [J].
Cobrinik, D .
ONCOGENE, 2005, 24 (17) :2796-2809
[7]   miRBase: tools for microRNA genomics [J].
Griffiths-Jones, Sam ;
Saini, Harpreet Kaur ;
van Dongen, Stijn ;
Enright, Anton J. .
NUCLEIC ACIDS RESEARCH, 2008, 36 :D154-D158
[8]   Loss of 9p leads to p16INK4A down-regulation and enables RB/E2F1-dependent cell cycle promotion in gastrointestinal stromal tumours (GISTs) [J].
Haller, F. ;
Loebke, C. ;
Ruschhaupt, M. ;
Cameron, S. ;
Schulten, H-J ;
Schwager, S. ;
von Heydebreck, A. ;
Gunawan, B. ;
Langer, C. ;
Ramadori, G. ;
Sueltmann, H. ;
Poustka, A. ;
Korf, U. ;
Fuezesi, L. .
JOURNAL OF PATHOLOGY, 2008, 215 (03) :253-262
[9]   Comprehensive MicroRNA Profiling for Head and Neck Squamous Cell Carcinomas [J].
Hui, Angela B. Y. ;
Lenarduzzi, Michelle ;
Krushel, Tiffaney ;
Waldron, Levi ;
Pintilie, Melania ;
Shi, Wei ;
Perez-Ordonez, Bayardo ;
Jurisica, Igor ;
O'Sullivan, Brian ;
Waldron, John ;
Gullane, Pat ;
Cummings, Bernard ;
Liu, Fei-Fei .
CLINICAL CANCER RESEARCH, 2010, 16 (04) :1129-1139
[10]  
Hummel R, 2011, TUMOR CENT NERV SYST, V3, P185, DOI 10.1007/978-94-007-1399-4_19