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
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.
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.