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MiR–206 inhibits proliferation, migration, and invasion of gastric cancer cells by targeting the MUC1 gene

Authors Deng M, Qin Y, Chen X, Wang Q, Wang J

Received 12 July 2018

Accepted for publication 12 October 2018

Published 25 January 2019 Volume 2019:12 Pages 849—859


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche

Min Deng,1 Yiyu Qin,2 Xiaodong Chen,3 Qizhi Wang,1 Jianchao Wang1

1Department of Gastroenterology, The First Affiliated Hospital, Bengbu Medical College, Bengbu, Anhui 233004, People’s Republic of China; 2Clinical Medical College, Research Centre of Biomedical Technology, Yancheng Institute of Health Sciences, Yancheng, Jiangsu 224005, People’s Republic of China; 3Department of Orthopedics, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, People’s Republic of China

Background: MicroRNAs (miRNAs) can regulate the post-transcriptional level of gene expression. It has been documented that downregulation of miR-206 is significant in human gastric cancer (GC), whereas its role in GC cell biological behaviors, including proliferation, migration, and invasion, has not been thoroughly investigated. MiR-206 levels have a negative association with lymph node metastasis and tumor invasion, and patients with higher miR-206 expression have better prognoses. Functional studies demonstrated that miR-206 overexpression significantly suppresses GC cell proliferation, migration, and invasion, and induces apoptosis in vitro.
Materials and methods: MiR-206 and MUC1 were determined by RNA extraction, quantitative real-time polymerase chain reaction, and luciferase reporter gene assays. The viability of GC cells was tested using the Cell Counting Kit 8 assay. Transwell invasion and migration assays detected GC cancer cell proliferation, invasion, and migration. Flow cytometry was applied to analyze apoptotic cells. FACS analysis was applied to detect the mitochondrial membrane potential of cells. Western blotting assay determined protein levels.
Results: The luciferase reporter gene assay demonstrated that miR-206 might directly bind to the 3'UTR of the MUC1 gene and suppress MUC1 expression. Furthermore, MUCI expression was upregulated and inversely associated with miR-206 levels in GC tissues. More importantly, the miR-206-mediated suppression of proliferation, migration, and invasion, and the induction of apoptosis, were abrogated by MUC1 overexpression.
Conclusion: Our data demonstrated that miR-206 may exert antitumor activities through inhibiting the expression of MUC1, which may serve as an effective and potential target for GC treatment.

Keywords: miR-206, MUC1, gastric cancer, metastasis

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