Open AccessLong Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion by Acting as a Competing Endogenous RNA of miR-19a
Author(s) -
Nan Qin,
Gui-Feng Tong,
Liwei Sun,
Xiaolin Xu
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504017x14886689179993
Subject(s) - competing endogenous rna , meg3 , tensin , glioma , pten , microrna , biology , carcinogenesis , cancer research , long non coding rna , cell growth , downregulation and upregulation , non coding rna , cancer , signal transduction , microbiology and biotechnology , gene , pi3k/akt/mtor pathway , genetics
Glioma, with varying malignancy grades and histological subtypes, is the most common primary brain tumor in adults. Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts and have been proven to play an important role in tumorigenesis. Our study aims to elucidate the combined effect of lncRNA maternally expressed gene 3 (MEG3) and microRNA-19a (miR-19a) in human glioma U87 and U251 cell lines. Real-time PCR revealed that MEG3 was downregulated and miR-19a was upregulated in malignant glioma tissues and cell lines. Bioinformatics analyses (TargetScan, miRanda, and starBase V2.0) showed that phosphatase and tensin homolog (PTEN) is a target of miR-19a with complementary binding sites in the 3'-UTR. As expected, luciferase results verified the putative target site and also revealed the complementary binding between miR-19a and MEG3. miR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration, and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis. Our study is the first to demonstrate that lncRNA MEG3 suppresses glioma cell proliferation, migration, and invasion by acting as a ceRNA of miR-19a, which provides a novel insight about the pathogenesis of glioma.