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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...

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Detalles Bibliográficos
Autores principales: Liu, Jia, Cao, Linggai, Zhao, Na, Feng, Yue, Yu, Ze, Li, Yuhua, Teng, Chunbo, Hu, Jifan, Li, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
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
Descripción
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.