cas2408-sup-0001-FigureS1.epsimage/eps1494KFig. S1. Left: Mutant and wild-type epidermal growth factor receptor (EGFR) plasmids were mixed at various ratios, then the mixed plasmids were amplified as a PCR template for fragment analyses. Calibration curve between mixture ratio of the plasmids and proportion ratio of amplified fragments. Right: Electropherograms of the fragment analysis of the mixtures of mutant and wild-type EGFR plasmids.
cas2408-sup-0002-FigureS2.epsimage/eps2094KFig. S2. Data for A549 cells are shown. (A) Left: Electropherograms of the fragment analyses. Right: Relative proportions of wild-type epidermal growth factor receptor (EGFR) expression. (B) Left: Gefitinib sensitivity curves. Right: IC50 values of cells to gefitinib. (C) Western blot analysis for total and phosphorylated EGFR, AKT, and ERK.
cas2408-sup-0003-FigureS3.epsimage/eps1500KFig. S3. (A) Direct sequencing of amplified fragment of exon 19 in epidermal growth factor receptor (EGFR) gene from PC9 cell-derived genomic DNA. (B) Copy numbers of EGFR gene were determined by quantitative PCR.
cas2408-sup-0004-FigureS4.epsimage/eps1578KFig. S4. (A) mRNA expression level of epidermal growth factor receptor (EGFR) ligands including EGF, epiregulin, amphiregulin, and TGFα in PC9 cells by quantitative PCR. (B) Hypoxia-inducible factor-1α (HIF1α) or transforming growth factor-α (TGFα) expression in HCC2935, A549, and HCC827 cells by Western blotting. (C) TGFα or HIF1α knockdown by siRNA reversed hypoxia-induced resistance to gefitinib in HCC2935 cells.
cas2408-sup-0005-FigureS5.epsimage/eps1685KFig. S5. Proposed model depicting the involvement of wild-type epidermal growth factor receptor (EGFR), hypoxia-inducible factor-1α (HIF1α), and transforming growth factor-α (TGFα) in hypoxia-induced resistance to gefitinib in PC9 cells.

Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.