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.