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miR‐577 inhibits glioblastoma tumor growth via the Wnt signaling pathway
Author(s) -
Zhang Weiguang,
Shen Chen,
Li Chenguang,
Yang Guang,
Liu Huailei,
Chen Xin,
Zhu Dan,
Zou Huichao,
Zhen Yunbo,
Zhang Daming,
Zhao Shiguang
Publication year - 2016
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22304
Subject(s) - wnt signaling pathway , biology , axin2 , lrp6 , lrp5 , cancer research , microrna , signal transduction , cyclin d1 , cell growth , u87 , transfection , microbiology and biotechnology , cell culture , cell , cell cycle , glioma , gene , genetics
microRNAs (miRNAs) are commonly altered in glioblastoma. Publicly available algorithms suggest the Wnt pathway is a potential target of miR‐577 and the Wnt pathway is commonly altered in glioblastoma. Glioblastoma has not been previously evaluated for miR‐577 expression. Glioblastoma tumors and cell lines were evaluated for their expression of miR‐577. Cell lines were transfected with miR‐577, miR‐577‐mutant, or control mimics to evaluate the effect of miR‐577 expression on cell proliferation in vitro and in an animal model. Wnt pathway markers were also evaluated for their association with miR‐577 expression. miR‐577 expression was decreased in 33 of 40 (82.5%) glioblastoma tumors and 5 of 6 glioblastoma cell lines. miR‐577 expression correlated negatively with cell growth and cell viability. miR‐577 down‐regulation was associated with increased expression of the Wnt signaling pathway genes lipoprotein receptor‐related protein (LRP) 6 (LRP6) and β‐catenin. Western blot analysis confirmed decreased expression of the Wnt signaling pathway genes Axin2, c‐myc, and cyclin D1 in miR‐577 transfected cells. miR‐577 expression is down‐regulated in glioblastoma. miR‐577 directly targets Wnt signaling pathway components LRP6 and β‐catenin . miR‐577 suppresses glioblastoma multiforme (GBM) growth by regulating the Wnt signaling pathway. © 2015 Wiley Periodicals, Inc.