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miR-338-3p inhibits A549 lung cancer cell proliferation and invasion by targeting AKT and β-catenin signaling pathways
The aim of the present study was to explore the underlying mechanism of microRNA-338-3p (miR-338-3p) in lung cancer cell (A549) invasion and proliferation. A microarray assay showed that miR-338-3p upregulated 216 and downregulated 147 genes in A549 cells, and the differentially expressed genes were...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6579971/ https://www.ncbi.nlm.nih.gov/pubmed/31115502 http://dx.doi.org/10.3892/mmr.2019.10215 |
Sumario: | The aim of the present study was to explore the underlying mechanism of microRNA-338-3p (miR-338-3p) in lung cancer cell (A549) invasion and proliferation. A microarray assay showed that miR-338-3p upregulated 216 and downregulated 147 genes in A549 cells, and the differentially expressed genes were enriched for several signaling pathways, including AKT and β-catenin signaling pathways. Western blotting results showed that phosphorylated (p)-AKT at Ser473 and at Thr308 and p-β-catenin at Ser552 were downregulated. Inhibiting AKT signaling pathway decreased β-catenin signaling pathway. Overexpression of β-catenin promoted the invasion of A549 cells. In addition, miR-338-3p showed inhibitory effect on the primary tumor developed from Kras(G12D) mice. Together, the data of the present study support that miR-338-3p inhibits lung cancer cell invasion and proliferation by downregulating AKT/β-catenin signaling pathway. The present findings supported the potential use of miR-338-3p in the treatment of lung cancer. |
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