NDLI: MicroRNA-219-5p exerts tumor suppressor function by targeting ROBO1 in glioblastoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jiang, Yongmei Yin, Lin Jing, Huirong Zhang, Hui
Description	Country affiliation: China Author Affiliation: Jiang Y ( Department of Neurology, Second Affiliated Hospital, Dalian Medical University, No. 467 Zhongshan Road, Dalian, Liaoning, 116027, China. zhuxufifa2007@163.com.); Yin L ( Department of Neurology, Second Affiliated Hospital, Dalian Medical University, No. 467 Zhongshan Road, Dalian, Liaoning, 116027, China. Lin_yin1@163.com.); Jing H ( Department of Neurology, Second Affiliated Hospital, Dalian Medical University, No. 467 Zhongshan Road, Dalian, Liaoning, 116027, China. Huirong_jing@163.com.); Zhang H ( Department of Neurology, Second Affiliated Hospital, Dalian Medical University, No. 467 Zhongshan Road, Dalian, Liaoning, 116027, China. Hui_zhang2014@163.com.)
Abstract	Previous studies have shown that miR-219-5p is dysregulated and exerts tumor-suppressive effects in cancer development and progression. However, the molecular function and mechanism of miR-219-5p in glioblastoma growth and invasion are still unclear. In the present study, we show that miR-219-5p was downregulated in a panel of glioma tissues with different grades and in all the human glioma cell lines examined. Ectopic expression of miR-219-5p inhibited proliferation and invasion and induced apoptosis in vitro, and xenograft formation in vivo. ROBO1 was found to be a direct target of miR-219-5p, and when overexpressed in miR-219-5p-expressing glioma cells, was able to restore proliferative and invasive ability. Finally, in vivo investigation confirmed that miR-219-5p was a tumor suppressor that regulated ROBO1 expression. Taken together, these studies demonstrate that miR-219-5p inhibited cancer cell growth and invasion by direct targeting ROBO1, implicating miR-219-5p as an attractive candidate for cancer therapy.
File Format	HTM / HTML
ISSN	10104283
Issue Number	11
Volume Number	36
e-ISSN	14230380
Journal	Tumor Biology
Language	English
Publisher	Springer
Publisher Date	2015-11-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Medicine__semicolon__oncology Cell Transformation, Neoplastic Genetics Glioblastoma Micrornas Nerve Tissue Proteins Biosynthesis Receptors, Immunologic Animals Apoptosis Cell Line, Tumor Cell Proliferation Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Pathology Humans Mice Neoplasm Invasiveness Antagonists & Inhibitors Xenograft Model Antitumor Assays Journal Article
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

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