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Environ Sci Pollut Res Int ; 25(18): 17674-17681, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29671226

ABSTRACT

Long non-coding RNAs (lncRNAs) LINC00152 plays important roles in the progression of some tumors. However, the role of LINC00152 in human l glioblastoma is still unknown. In this study, we indicated that LINC00152 expression level was upregulated in glioblastoma tissues and cell lines. Overexpression of LINC00152 promoted the U87 and LN229 cell proliferation and invasion. Moreover, overexpression of LINC00152 suppressed the E-cadherin expression, where ectopic expression of LINC00152 promoted the N-cadherin, Vimentin, and Snail expression. These results suggested that LINC00152 enhanced epithelial-to-mesenchymal transition (EMT) program in the glioblastoma cell. Overexpression of LINC00152 suppressed the miR-107 expression in the U87 cell and enhanced the HMGA2 expression, which is a direct target gene of miR-107. In addition, we showed that the miR-107 expression was downregulated in the glioblastoma tissues and cell lines. Interesting, the expression of LINC00152 was negatively related with miR-107 expression in the glioblastoma tissues. Furthermore, LINC00152 promoted the glioblastoma cell proliferation and invasion through inhibiting miR-107 expression. These data suggested that LINC00152 acted as oncogene roles in the glioblastoma cell partly through targeting the miR-107 expression.


Subject(s)
Cadherins/metabolism , Glioblastoma , MicroRNAs/genetics , RNA, Long Noncoding/genetics , Antigens, CD , Cadherins/chemistry , Cell Proliferation , Disease Progression , Down-Regulation , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Humans , MicroRNAs/chemistry , Up-Regulation
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