Figure 6 — MET inhibitor, capmatinib overcomes osimertinib resistance via suppression of MET/Akt/snail signaling in non-small cell lung cancer and decreased generation of cancer-associated fibroblasts

Research Paper|Volume 13, Issue 5|pp. 6890–6903

MET inhibitor, capmatinib overcomes osimertinib resistance via suppression of MET/Akt/snail signaling in non-small cell lung cancer and decreased generation of cancer-associated fibroblasts

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Figure 6.Cancer associated fibroblasts (CAFs) from osimertinib-resistant patients promoted osimertinib resistance via HGF/MET signaling and induction of epithelial-to-mesenchymal transition (EMT) and transformed NSCLC cells into TKI resistant stem-like cells. The treatment of capmatinib (MET inhibitor) inhibited CAF-mediated MET/Akt activation bypassing EGFR signaling pathway and re-sensitizing NSCLC towards osimertinib.