Mn12Ac inhibits the migration, invasion and epithelial-mesenchymal transition of lung cancer cells by downregulating the Wnt/β-catenin and PI3K/AKT signaling pathways

• Published in: Oncology letters Vol. 16; no. 3; pp. 3943 - 3948
• Main Authors: Chen, Zihao, He, Jiangbo, Xing, Xiqian, Li, Ping, Zhang, Wei, Tong, Zhuxiu, Jing, Xiaojie, Li, Licheng, Liu, Dian, Wu, Qiong, Ju, Hongping
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.09.2018; D.A. Spandidos
• Subjects: Biotechnology; Cell adhesion & migration; Drug resistance; Gene expression; Immunoglobulins; Kinases; Ligands; Lung cancer; Metastasis; Morphology; Mortality; Oncology; Proteins; Studies; Transcription factors; United States > US; Germany; migration; epithelial-mesenchymal transition; Wnt; phosphoinositide 3-kinase; manganese-12 acetate
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2018.9136

Lung cancer is the leading cause of global cancer-associated mortality, therefore it is important to reveal the molecular mechanisms of lung cancer progression and to develop novel therapeutic targets. The results of the present study identified that manganese-12 acetate (Mn12Ac) was able to significantly inhibit the migration and invasion of A549 cells. Western blotting demonstrated that treatment with Mn12Ac was able to upregulate E-cadherin, and downregulate N-cadherin and vimentin. It was also identified by a quantitative polymerase chain reaction analysis that Mn12Ac was able to reduce the mRNA expression levels of EMT-associated transcription factors Snail, Slug, Twist-related protein 1 and zinc finger E-box-binding homeobox 1. It was also demonstrated that Mn12Ac was able to reduce the expression levels of Wnt and β-catenin proteins, and suppress the phosphorylation of phosphoinositide 3-kinase (PI3K) and AKT in A549 cells. Notably, it was revealed that Mn12Ac was able to decrease the mRNA and protein expression levels of programmed death ligand-1. Taken together, the results suggested that Mn12Ac is able to inhibit cell migration, invasion and EMT in lung cancer cells by regulating the Wnt/β-catenin and PI3K/AKT signaling pathways.