MNX1-AS1 accelerates the epithelial-mesenchymal transition in osteosarcoma cells by activating MNX1 as a functional oncogene

F. Wu, Y. Zhong, X.-B. Lang, Y.-L. Tu, S.-F. Sun

Department of Traditional Chinese Medicine, First People’s Hospital of Fuyang District, Hangzhou, China. wufangdoc@yeah.net

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• Oncology

OBJECTIVE: To investigate whether MNX1-AS1 can accelerate epithelial-mesenchymal transition (EMT) of osteosarcoma cells via activating MNX1.

PATIENTS AND METHODS: The expression pattern of MNX1-AS1 in osteosarcoma tissues and cell lines was examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the cytoplasmic and nuclear levels of MNX1-AS1 in osteosarcoma cells were also determined. The regulatory effects of MNX1-AS1 on viability, clonality, migratory, and invasive abilities of the osteosarcoma cells were evaluated. The relative levels of MNX1 and EMT-related genes influenced by MNX1-AS1 were detected. The methylation ability in the promoter of the osteosarcoma cells transfected with si-MNX1-AS1 or MNX1-AS1 vector was determined by the whole genome bisulfite sequencing.

RESULTS: MNX1-AS1 was upregulated in osteosarcoma tissues and cell lines, which was mainly expressed in the nucleus. The knockdown of MNX1-AS1 markedly attenuated viability, clonality, migratory, and the invasive abilities of the osteosarcoma cells. Besides, the transfection of si-MNX1-AS1 in U2OS and MG63 cells downregulated MNX1 and Snail, and upregulated E-cadherin. The methylation ability increased after the knockdown of MNX1-AS1, while the overexpression of MNX1-AS1 obtained the opposite trends.

CONCLUSIONS: MNX1-AS1 mediates EMT of the osteosarcoma cells via activating MNX1, thereafter accelerating the progression of the osteosarcoma.

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