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Retracted : Knockdown of lncRNA MEG3 inhibits viability, migration, and invasion and promotes apoptosis by sponging miR‐127 in osteosarcoma cell
Author(s) -
Wang Yang,
Kong Daliang
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26230
Subject(s) - meg3 , gene knockdown , viability assay , cell growth , apoptosis , cancer research , cell culture , transfection , metastasis , downregulation and upregulation , osteosarcoma , cell migration , cell , wnt signaling pathway , biology , chemistry , microbiology and biotechnology , signal transduction , long non coding rna , gene , cancer , genetics
Osteosarcoma (OS) is one of the most common bone malignancies and occurs almost exclusively in children and adolescents. This study aimed to explore the role of lncRNA maternally expressed gene 3 (MEG3) in OS cells growth and metastasis, and to uncover the possible underlying mechanism. In this study, the expressions of MEG3 in five OS cell lines (MG63, OS‐732, SaOS, G292, and 143B) and in a human osteoblast cell line hFOB1.19 were measured by qRT‐PCR analysis. The expressions of MEG3, miR‐127, and ZEB1 in OS‐732 cells were overexpressed or suppressed by transfection. Cell viability, migration, invasion, and apoptosis were then assessed. The results showed that MEG3 was highly expressed in OS cell lines when compared to hFOB1.19 cell. MEG3 silence significantly suppressed OS‐732 cells growth and metastasis, as evidenced by the decreases in cell viability, migration, invasion, and increase in apoptotic cell rate. MEG3 acted as an endogenous sponge by binding to miR‐127. More interestingly, MEG3 silence could not suppress OS‐732 cells growth and metastasis when miR‐127 was knocked down. ZEB1 was a target gene of miR‐127, and miR‐127 overexpression‐induced impairments in cell growth and metastasis were attenuated when ZEB1 was overexpressed. Moreover,miR‐127 suppression activated JNK and Wnt signaling pathways, while these activations were recovered by ZEB1 silence. To conclude, our findings suggest that lncRNA MEG3 promoted OS cells growth and metastasis in vitro through sponging miR‐127. This study provides the evidence that MEG3 may be a potential therapeutic target for OS.