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. 2022 Apr 13;23(6):170. doi: 10.3892/ol.2022.13290

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Copyright: © Jing et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 6. — Tepotinib inhibits proliferation, migration, and invasion of WM451 cells by restraining the activation of MET and PI3K/AKT signaling pathways. (A) The proliferation of WM451 cells treated with or without 10 ng/ml tepotinib and 50 ng/ml HGF was detected using the MTT assay. (B) The migratory activity of WM451 cells treated with or without 10 ng/ml tepotinib and 50 ng/ml HGF was assessed using the wound healing assay. Magnification, ×100. (C) The invasive activity of WM451 cells treated with or without 10 ng/ml tepotinib and 50 ng/ml HGF was detected using the Transwell assay. Magnification, ×100. (D) The expression levels of the EMT-related proteins in WM451 cells treated with or without 10 ng/ml tepotinib and 50 ng/ml HGF were detected using western blot analysis. **P<0.01 and ***P<0.001 vs. control (DMSO) group; ^#P<0.05, ^##P<0.01 and ^###P<0.001 vs. tepotinib. MET, MET proto-oncogene, receptor tyrosine kinase; EMT, epithelial-mesenchymal transition; HGF, hepatocyte growth factor.