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miR-630 Inhibits Epithelial-to-Mesenchymal Transition (EMT) by Regulating the Wnt/β-Catenin Pathway in Gastric Cancer Cells
Despite availability of different treatments, gastric cancer remains the second highest cause of cancer-related deaths worldwide. This study was aimed to explore the role of miR-630 in gastric cancer by investigating the underlying mechanism of inhibiting epithelial-to-mesenchymal transition (EMT) o...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cognizant Communication Corporation
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848419/ https://www.ncbi.nlm.nih.gov/pubmed/29422112 http://dx.doi.org/10.3727/096504018X15178732625479 |
Sumario: | Despite availability of different treatments, gastric cancer remains the second highest cause of cancer-related deaths worldwide. This study was aimed to explore the role of miR-630 in gastric cancer by investigating the underlying mechanism of inhibiting epithelial-to-mesenchymal transition (EMT) of SGC-7901 and BGC-823 cells through the Wnt/β-catenin pathway. Results showed that miR-630 was downregulated in several gastric cancer cell lines, including SGC-7901 and BGC-823. Transfection of miR-630 mimic showed a significant decrease in wound healing in a scratch assay in both cell lines compared to a scramble group. Also, transfection of miR-630 mimic inhibited cell viability, migration, and invasion of gastric cancer cells. miR-630 mimic transfection suppressed EMT by activating the Wnt/β-catenin pathway. This was supported by the fact that miR-630-mediated suppression of the EMT phenotype was reversed in the presence of the Wnt/β-catenin inhibitor ICG001. miR-630 plays a protective role against gastric cancer by suppressing EMT through activating the Wnt/β-catenin pathway. |
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