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. 2020 Apr 8;44(1):185–195. doi: 10.3892/or.2020.7579

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Copyright: © Du 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 7. — The miR-625-3p/AXL axis contributes to gefitinib resistance via the SMAD pathway. (A) Western blot analysis of AXL, phosphorylated (p)-AXL, Smad3, p-Smad3, ZEB1, Snail, MMP2, and MMP9 expression in the parental HCC827GR cells compared to HCC827 cells or in cells after transfection of miR-625-3p mimic or knockdown of AXL. (B) A diagram of the mechanism of miR-625-3p/AXL-mediated gefitinib resistance. Gas6, growth arrest specific 6; TGFβ, transforming growth factor β; AXL, AXL receptor tyrosine kinase;; ZEB1, zinc finger E-box binding homeobox 1; MMP, matrix metalloproteinases; Snail, Snail family transcriptional repressor 1; p, phorphorylation; EMT, epithelial to mesenchymal transition.