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

Osimertinib resistant clinical samples of CAF increased oncogenic properties in NSCLC cells. (A) Cell viability assay showed that CAF-coculture led to an increased osimertinib in both H1975 and HCC827 cells as compared to their parental counterparts. In the presence of CAFs, both H1975 and HCC827 cells exhibited a significantly enhanced ability to form colonies (B) migrate (C) and generate tumor spheres (D). (E) Western blots analysis of CAF-cocultured H1975 and HCC827 cells indicated a prominently increased activity of EGFR, MET, elevated expression of EMT markers, vimentin and MMP9, stemness marker, β-catenin.

Figure 1. Osimertinib resistant clinical samples of CAF increased oncogenic properties in NSCLC cells. (A) Cell viability assay showed that CAF-coculture led to an increased osimertinib in both H1975 and HCC827 cells as compared to their parental counterparts. In the presence of CAFs, both H1975 and HCC827 cells exhibited a significantly enhanced ability to form colonies (B) migrate (C) and generate tumor spheres (D). (E) Western blots analysis of CAF-cocultured H1975 and HCC827 cells indicated a prominently increased activity of EGFR, MET, elevated expression of EMT markers, vimentin and MMP9, stemness marker, β-catenin.