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. 2018 Jan 8;9(3):353–359. doi: 10.1111/1759-7714.12584

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© 2018 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Manganese‐12 acetate (Mn12Ac) inhibited the Wnt/β‐catenin and PI3K/AKT signaling pathways, and decreased the programmed cell death ligand 1 (PD‐L1) expression. (a) Protein expressions of Wnt1 and β‐catenin were accessed by western blotting analysis. (b) Phosphorylation of PI3K and AKT were accessed by western blotting analysis. (c) Protein expression of PD‐L1 was accessed by western blotting assay. (d) mRNA expression of PD‐L1 was accessed by real‐time PCR assay. MCF7, MDA‐MB‐231. NC, negative control.

Inline graphic — Manganese‐12 acetate (Mn12Ac) inhibited the Wnt/β‐catenin and PI3K/AKT signaling pathways, and decreased the programmed cell death ligand 1 (PD‐L1) expression. (a) Protein expressions of Wnt1 and β‐catenin were accessed by western blotting analysis. (b) Phosphorylation of PI3K and AKT were accessed by western blotting analysis. (c) Protein expression of PD‐L1 was accessed by western blotting assay. (d) mRNA expression of PD‐L1 was accessed by real‐time PCR assay. MCF7, MDA‐MB‐231. NC, negative control.